{"service":"Mito.news","version":"1.1.9","updated_at":"2026-09-07T02:17:21.045Z","count":50,"corpus_count":104,"free":true,"spotlight":false,"product_sold":"mitos_importance_article","purpose":"Mito.news: mitochondria importance briefs on bioRxiv/medRxiv. Free HTML for humans; agents buy structured JSON (batch papers, single paper, editorial digest, search) via x402 USDC on Base.","paid_sku_count":4,"note":"Bot start here. Sorted by importance_score. Humans: free HTML at https://mito.news/articles/{id}. Spotlight: GET /api/v1/catalog?spotlight=1 (top 20). Bots: four x402 SKUs in paid_endpoints.","papers":[{"id":"10-64898-2026-08-12-744403","doi":"10.64898/2026.08.12.744403","title":"Neuroinflammation and metabolic dysfunction in POLG-related mitochondrial epilepsy","headline":"POLG occipital epilepsy is an immunometabolic lesion: OXPHOS collapse meets innate inflammation in visual cortex","blurb":"In 12 post-mortem POLG-related epilepsy brains, occipital cortex (BA17) loses mitochondrial proteins and gains an innate-immune proteome, including OXPHOS-poor microglia. Control visual cortex is already richer in…","why_bots_should_care":"This is rare human neuropathology of a canonical mtDNA-maintenance epilepsy: paired BA17 vs BA9 proteomics plus glial immunohistochemistry. Use it as a regional-vulnerability and microglia-OXPHOS reference, not as a treatment claim.","key_claims":["Post-mortem occipital (BA17) and, less so, frontal (BA9) cortex from 12 POLG epilepsy patients (ages 3–28) show decreased mitochondrial protein abundance and increased innate-immune/inflammatory proteins versus matched controls.","Immunohistochemistry validates higher densities of CRP, osteopontin, serpin A3, CD14, HLA-DR, YKL40, TNF-alpha, and TSPO-positive cells.","POLG patient microglia have reduced OXPHOS subunit expression, linking glial mitochondrial failure to the inflammatory signature."],"confidence":"high","keywords":["POLG","status epilepticus","occipital cortex","microglia","TSPO","OXPHOS","neuroinflammation"],"dysfunction_signals":["OXPHOS subunit loss in tissue and microglia","innate neuroinflammation (TNF, HLA-DR, TSPO, YKL40)","region-selective cortical vulnerability (occipital > frontal)","POLG-related mtDNA maintenance disease"],"server":"biorxiv","posted_date":"2026-08-14","authors_short":"Smith LA, Wilson M, Elsaid EM et al.","categories":[],"topics":["OXPHOS","metabolism","neurobiology","immunology","mtDNA"],"importance_score":94,"url":"https://www.biorxiv.org/content/10.64898/2026.08.12.744403","free_html_url":"https://mito.news/articles/10-64898-2026-08-12-744403","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-12-744403","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-24-746860","doi":"10.64898/2026.08.24.746860","title":"NLRX1 is an essential, druggable regulator of mitochondrial permeability transition","headline":"NLRX1 is the CypD-independent handle on the mitochondrial permeability transition pore","blurb":"Two chemically unrelated, brain-penetrant inhibitors of the mitochondrial permeability transition pore (mPTP) bind the mitochondrial NOD-like receptor NLRX1, and binding potency tracks pore blockade. Loss of NLRX1…","why_bots_should_care":"The pore's molecular identity has been a decades-long deadlock. This preprint supplies a shared protein target for two optimized chemotypes, genetic necessity in human cells and mouse tissue, physical association with ATP synthase and the adenine nucleotide translocase, and a…","key_claims":["Affinity-based chemoproteomics with two structurally distinct, optimized, brain-penetrant mPTP-inhibitor chemotypes identifies NLRX1 as their shared target.","Binding potency across a compound series tracks mPTP-inhibitory activity, arguing the interaction is on-pathway rather than a promiscuous off-target.","CRISPR-Cas9 loss of NLRX1 in human cells, and Nlrx1 deletion in mouse tissues, raises the calcium threshold for pore opening; overexpression lowers it. Both effects are CypD-independent."],"confidence":"high","keywords":["NLRX1","mPTP","cyclophilin D","GSK900","ATP synthase","adenine nucleotide translocase","chemoproteomics"],"dysfunction_signals":["mitochondrial permeability transition","calcium overload","CypD-independent pore opening","neurological injury","mitochondrial proteostasis"],"server":"biorxiv","posted_date":"2026-08-26","authors_short":"Peltier-Heap R, Frederick DW, Pickering RJ et al.","categories":[],"topics":["calcium signaling","therapeutics","apoptosis","neurobiology","OXPHOS"],"importance_score":93,"url":"https://www.biorxiv.org/content/10.64898/2026.08.24.746860","free_html_url":"https://mito.news/articles/10-64898-2026-08-24-746860","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-24-746860","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-12-744280","doi":"10.64898/2026.08.12.744280","title":"Respiration-Deficient Cells Require Pyruvate Carboxylase to Suppress Asparagine Auxotrophy","headline":"Past 70% mtDNA heteroplasmy, cells need pyruvate carboxylase — or exogenous asparagine — to keep translating","blurb":"Isogenic mtDNA-deletion lines show linear loss of respiration with heteroplasmy, but redox stress, ISR, and translation failure only after discrete thresholds (~50% and ~70%). Those late defects reverse with asparagine…","why_bots_should_care":"A clean heteroplasmy titration that separates respiration, redox, ISR, and anaplerosis. It also gives a metabolic-therapy hook: PC expression as a biomarker for asparagine dependence / asparaginase sensitivity in OXPHOS-deficient tumors.","key_claims":["In isogenic cells with similar mtDNA deletions, respiration falls linearly as heteroplasmy rises.","Cellular redox imbalance stays muted until heteroplasmy exceeds ~50%; ISR and impaired translation appear past ~70%.","Asparagine supplementation or pyruvate carboxylase overexpression reverses the high-heteroplasmy translation/ISR defects."],"confidence":"high","keywords":["heteroplasmy","pyruvate carboxylase","asparagine","asparaginase","ISR","mtDNA deletion","anaplerosis"],"dysfunction_signals":["mtDNA deletion heteroplasmy","ETC/respiration collapse","ISR and translation failure","asparagine auxotrophy","low pyruvate carboxylase"],"server":"biorxiv","posted_date":"2026-08-13","authors_short":"Cui R, Ryu KW, Fu Y et al.","categories":[],"topics":["mtDNA","OXPHOS","metabolism","cancer","therapeutics","genetics"],"importance_score":92,"url":"https://www.biorxiv.org/content/10.64898/2026.08.12.744280","free_html_url":"https://mito.news/articles/10-64898-2026-08-12-744280","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-12-744280","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-12-744345","doi":"10.64898/2026.08.12.744345","title":"Clever-1 blockade disrupts lipid metabolism and mitochondrial fitness in acute myeloid leukemia","headline":"Clever-1 sits on AML mitochondria, feeds complex IV with lipoprotein lipid, and is a bexmarilimab-sensitive OXPHOS liability","blurb":"Clever-1 is not only an immune scavenger receptor. In AML it localizes to mitochondria, associates with ATAD3, delivers lipoprotein-derived lipid, and supports complex IV assembly, cristae, and spare respiratory…","why_bots_should_care":"A clinically used anti–Clever-1 antibody is being repositioned from immuno-oncology to leukemia-cell mitochondrial metabolism. Pair this with AML OXPHOS-high signatures, ATAD3/complex IV assembly machinery, and lipid-restricted culture conditions.","key_claims":["Clever-1 inhibition with bexmarilimab drives early mitochondrial transcriptional reprogramming and then suppresses OXPHOS in AML cell lines.","Immunoelectron microscopy places Clever-1 at mitochondria; proteomics shift its association with mitochondrial-linked proteins including ATAD3.","Blockade reduces mitochondrial delivery of lipoprotein-derived lipids and selectively remodels mitochondrial lipid composition."],"confidence":"high","keywords":["Clever-1","bexmarilimab","AML","ATAD3","complex IV","lipoprotein lipid","spare respiratory capacity"],"dysfunction_signals":["OXPHOS suppression after Clever-1 blockade","complex IV assembly failure","cristae disruption","dysfunctional mitochondria accumulation","impaired mitochondrial lipid delivery"],"server":"biorxiv","posted_date":"2026-08-12","authors_short":"Ylitalo A, Mickos J, Hakoniemi M et al.","categories":[],"topics":["OXPHOS","metabolism","redox biology","therapeutics","cancer"],"importance_score":91,"url":"https://www.biorxiv.org/content/10.64898/2026.08.12.744345","free_html_url":"https://mito.news/articles/10-64898-2026-08-12-744345","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-12-744345","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-21-26361041","doi":"10.64898/2026.08.21.26361041","title":"A Scalable Framework for Harmonized mtDNA Analysis Across Diverse Biobanks","headline":"251,512 biobank genomes already held mitochondrial DNA. This pipeline finally calls it.","blurb":"A portable Mitoverse mtDNA-Server 2 Fusion workflow, run natively at Mount Sinai (54,151 whole-exome participants) and reimplemented under All of Us Workbench constraints (197,361 whole-genome participants), produced…","why_bots_should_care":"Most nuclear-first biobanks sit on unused mitochondrial reads. This paper is the implementation pattern for unlocking them: Fusion of GATK Mutect2 plus mutserve2, 3% heteroplasmy floor, NUMT-aware quality control, haplogroup assignment, and a cloud rewrite when Docker/Nextflow…","key_claims":["The same Fusion analytical strategy (Mutect2 + mutserve2, 3% heteroplasmy detection limit, contamination and haplogroup annotation) was deployed in two incompatible compute environments.","Mount Sinai Million whole-exome data from 54,151 participants yielded 3,497,139 variant observations (16,128 unique variants; mean 64.6 per person; median depth 410×).","All of Us whole-genome data from 197,361 participants yielded 9,461,434 variant observations (34,142 unique variants; mean 47.9 per person; median depth 2,401×)."],"confidence":"high","keywords":["mtDNA","heteroplasmy","Mitoverse","All of Us","Mount Sinai Million","Mutect2","mutserve2","NUMTs"],"dysfunction_signals":["heteroplasmy","rare mtDNA variants","NUMT contamination","missing biobank mtDNA call sets"],"server":"medrxiv","posted_date":"2026-08-25","authors_short":"Schecter DR, Lee SS, Vimal T et al.","categories":[],"topics":["mtDNA","genetics","metabolism"],"importance_score":90,"url":"https://www.medrxiv.org/content/10.64898/2026.08.21.26361041","free_html_url":"https://mito.news/articles/10-64898-2026-08-21-26361041","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-21-26361041","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-19-745859","doi":"10.64898/2026.08.19.745859","title":"The HES1-SOD1 Antagonism Shapes Senescence Heterogeneity and Impacts Metastatic Relapse of Circulating Tumor Cells","headline":"HES1-low senescent CTCs keep OXPHOS and SOD1 — and those are the cells that regrow metastases","blurb":"Senescence in circulating tumor cells is not one state. HES1-low senescent CTCs keep mitochondrial fitness, oxidative phosphorylation, and SOD1-dependent ROS detox, and they regrow tumors more efficiently than HES1-high…","why_bots_should_care":"This paper links a transcription-factor split (HES1 high vs low) to a mitochondrial fitness split (OXPHOS/SOD1 on vs off) inside senescent CTCs, then to metastatic relapse and a two-drug combination. Agents tracking CTC biology, senescence, SOD1, or tumor OXPHOS should ingest…","key_claims":["Cortactin-knockdown CTC senescence plus single-cell multi-omics split senescent CTCs into HES1-low and HES1-high subpopulations with distinct evolutionary trajectories and metabolic signatures.","HES1-low senescent CTCs showed enhanced mitochondrial fitness, OXPHOS, and ROS-detoxifying capacity, and they regrew tumors more efficiently with a pro-inflammatory, thrombotic phenotype.","HES1 bound the Sod1 promoter and repressed SOD1, producing redox imbalance and mitochondrial dysfunction tied to weaker tumor-regrowth capacity."],"confidence":"high","keywords":["HES1","SOD1","circulating tumor cells","senescence","OXPHOS","ABT737","metastasis","melanoma"],"dysfunction_signals":["oxphos_heterogeneity","ros_imbalance","sod1_repression","senescence","apoptosis_dependence"],"server":"biorxiv","posted_date":"2026-08-20","authors_short":"Huang G, Xu X, Zhang B et al.","categories":[],"topics":["cancer","OXPHOS","redox biology","therapeutics","aging"],"importance_score":89,"url":"https://www.biorxiv.org/content/10.64898/2026.08.19.745859","free_html_url":"https://mito.news/articles/10-64898-2026-08-19-745859","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-19-745859","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744045","doi":"10.64898/2026.08.14.744045","title":"Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER Stress","headline":"MICOS Chchd3 loss breaks the fly heart through mitophagy, ROS, and ER stress — not ROS alone","blurb":"Cardiac knockdown of the MICOS subunit Chchd3 in Drosophila raises ROS and ER stress and genetically depends on Pink1/parkin mitophagy. Catalase overexpression fully normalizes ROS but only partly restores…","why_bots_should_care":"This is a clean genetic dissection of how a cristae-organization subunit becomes a cardiac phenotype. Track it if you map MICOS/CHCHD3/CHCHD6 to congenital heart disease, model Pink1/parkin buffering of cristae failure, or need a counterexample to ROS-equals-dysfunction scoring…","key_claims":["Chchd3 and Chchd6 are MICOS paralogs flagged as congenital-heart-disease candidate genes; the fly has one Chchd3/6 ortholog.","Moderate reduction of Pink1/parkin-mediated mitophagy synergistically worsens cardiac Chchd3 knockdown, implying the damaged organelle pool is being cleared and that clearance is load-bearing.","Chchd3 knockdown raises cardiac ROS and ER stress."],"confidence":"high","keywords":["CHCHD3","MICOS","Pink1","parkin","catalase","Xbp1","Drosophila heart","congenital heart disease"],"dysfunction_signals":["MICOS/cristae organization failure","impaired contractility","ROS elevation","ER stress","mitophagy interaction"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Dondi C, Ge S, Marchant JL et al.","categories":[],"topics":["mitochondrial dynamics","mitophagy","redox biology","cardiovascular","genetics"],"importance_score":88,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744045","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744045","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744045","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744765","doi":"10.64898/2026.08.14.744765","title":"In vitro fertilisation and vitrification disrupt embryo mitochondrial function and redox balance that persists into adulthood in mice","headline":"IVF and vitrification depolarize the blastocyst mitochondrion; the adult mouse heart still shows the bioenergetic scar","blurb":"Mouse IVF and embryo vitrification are separable mitochondrial injuries. Both lower blastocyst ΔΨm and glutathione; ROS is highest in vitrified IVF embryos. After transfer, adult left-ventricular mitochondria have less…","why_bots_should_care":"First adult-offspring cardiac mitochondrial physiology the authors know of after IVF/vitrification. Useful for ART-safety, DOHaD, and mitochondrial programming literatures. Species is mouse; do not translate into clinic-facing risk percentages.","key_claims":["IVF reduced blastocyst total, trophectoderm and inner-cell-mass counts; vitrification lowered ICM proportion and raised apoptosis.","Both IVF and vitrification depolarized mitochondria and depleted glutathione; ROS showed an interaction and was highest in vitrified IVF embryos.","IVF reduced live-birth rate and litter size; vitrification altered postnatal growth."],"confidence":"high","keywords":["IVF","vitrification","ART","blastocyst","cardiac mitochondria","glutathione","developmental programming"],"dysfunction_signals":["blastocyst ΔΨm depolarization","glutathione depletion and ROS increase","adult OXPHOS capacity loss","elevated cardiac H2O2","reduced complex I/III/IV activity"],"server":"biorxiv","posted_date":"2026-08-15","authors_short":"Chen Y, Chukwuefe HN, Zi M et al.","categories":[],"topics":["OXPHOS","redox biology","apoptosis","metabolism","cardiovascular"],"importance_score":88,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744765","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744765","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744765","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-07-743508","doi":"10.64898/2026.08.07.743508","title":"Mitochondrial Metabolism and Calcium Handling in Parkinson's Disease hiPSC-derived Astrocytes","headline":"LRRK2 astrocytes extrude calcium slowly; PRKN astrocytes run hotter OXPHOS; both fragment mitochondria","blurb":"Parkinson’s hiPSC astrocytes are not a single mitochondrial phenotype. LRRK2 G2019S cells hold less cytosolic calcium and extrude it more slowly after ATP. PRKN mutant astrocytes run a more oxidative bioenergetic…","why_bots_should_care":"Kowaltowski and colleagues give genotype-resolved astrocyte mitochondria — calcium, OCR, morphology, DRP1, complex abundance — in LRRK2 versus PRKN versus control hiPSC lines. Agents modeling PD as a glial bioenergetic disease should stop averaging those genotypes and should…","key_claims":["LRRK2 G2019S patient-derived astrocytes had lower intracellular calcium and slower calcium extrusion after ATP stimulation than control astrocytes (Fura-2 AM).","MitoTracker imaging showed increased mitochondrial fragmentation and peripheral redistribution in both LRRK2 and PRKN mutant astrocytes.","PRKN mutant astrocytes (c.155delA; Ex3-4del) exhibited a more oxidative bioenergetic phenotype than LRRK2 mutant astrocytes on continuous OCR monitoring (Resipher)."],"confidence":"high","keywords":["Parkinson","LRRK2","PRKN","parkin","astrocytes","hiPSC","calcium","DRP1"],"dysfunction_signals":["calcium_extrusion_delay","mitochondrial_fragmentation","drp1_phosphorylation","respiratory_complex_loss","oxphos_tone_shift"],"server":"biorxiv","posted_date":"2026-08-13","authors_short":"Cavalcante GC, Caldeira da Silva CC, Vogt ÉL et al.","categories":[],"topics":["neurobiology","calcium signaling","OXPHOS","mitochondrial dynamics","metabolism"],"importance_score":88,"url":"https://www.biorxiv.org/content/10.64898/2026.08.07.743508","free_html_url":"https://mito.news/articles/10-64898-2026-08-07-743508","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-07-743508","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-10-743872","doi":"10.64898/2026.08.10.743872","title":"Monitoring fatty acid trafficking during Drosophila melanogaster oogenesis reveals a role for the triglyceride synthase DGAT1 in protecting mitochondrial integrity","headline":"DGAT1 lipid droplets shield nurse-cell mitochondria — without them, fatty acids flood in and oogenesis arrests","blurb":"Drosophila nurse-cell mitochondria oxidize fatty acids in a stage-dependent way, peaking at mid-oogenesis, and they draw that fuel from ATGL-released lipid-droplet triglyceride. Blocking droplet formation with DGAT1…","why_bots_should_care":"This is a trafficking paper, not a \"lipids are good\" paper. It separates LD-derived FAO (ATGL-dependent membrane potential and oxidation) from LD-as-buffer (DGAT1 loss causes mitochondrial FA overload and developmental arrest). Use it to annotate DGAT1/ATGL/CPT-type import as a…","key_claims":["Nurse-cell mitochondria catabolize fatty acids in a stage-dependent manner, with FAO peaking in mid-oogenesis.","Fluorescent fatty acids fed to explanted follicles massively enrich in lipid droplets.","ATGL triglyceride-lipase mutants reduce mitochondrial membrane potential and FAO, implying mitochondria burn LD-derived fatty acids."],"confidence":"high","keywords":["DGAT1","ATGL","lipid droplets","fatty acid oxidation","oogenesis","Drosophila","lipotoxicity"],"dysfunction_signals":["mitochondrial fatty-acid overload","lipotoxicity","loss of membrane potential","reduced FAO","developmental arrest"],"server":"biorxiv","posted_date":"2026-08-12","authors_short":"White RP, Kilwein MD, Welte MA","categories":[],"topics":["metabolism","OXPHOS","mitochondrial dynamics","genetics"],"importance_score":87,"url":"https://www.biorxiv.org/content/10.64898/2026.08.10.743872","free_html_url":"https://mito.news/articles/10-64898-2026-08-10-743872","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-10-743872","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-10-743339","doi":"10.64898/2026.08.10.743339","title":"TR-107, a novel mitochondrial ClpP agonist, induces robust antitumor activity against preclinical models of adrenocortical carcinoma","headline":"ClpP agonist TR-107 collapses ACC respiration at nanomolar doses and synergizes with IGF-1R blockade","blurb":"TR-107, a selective agonist of the mitochondrial protease ClpP, kills adrenocortical carcinoma cells and patient-derived organoids at nanomolar concentrations by wrecking oxidative phosphorylation. Oxygen consumption…","why_bots_should_care":"ACC is a rare, mitochondria-intensive steroidogenic cancer with few drugs. This preprint names a ClpP agonist, a metabolic endpoint (OCR), a resistance-relevant property (not pumped by P-glycoprotein), and a rational combination (IGF-1R). Oncology and mitochondrial-proteostasis…","key_claims":["TR-107 produced nanomolar, dose-dependent cytotoxicity in NCI-H295R and mACC3 ACC lines and in short-term ACC patient-derived organoids, cutting viability and confluency.","Metabolic assays showed impaired oxygen consumption, disrupted oxidative phosphorylation, and lower basal respiration.","ROS rose in a dose-dependent manner and proteins that set the ferroptotic rheostat were upregulated."],"confidence":"high","keywords":["TR-107","ClpP","adrenocortical carcinoma","OXPHOS","IGF-1R","ABCB1","ferroptosis","organoids"],"dysfunction_signals":["clpp_hyperactivation","oxphos_collapse","ros_increase","ferroptosis_rheostat","proteostasis_failure"],"server":"biorxiv","posted_date":"2026-08-11","authors_short":"Karadimov GI, Kim YS, Fu H et al.","categories":[],"topics":["cancer","therapeutics","OXPHOS","redox biology","metabolism"],"importance_score":87,"url":"https://www.biorxiv.org/content/10.64898/2026.08.10.743339","free_html_url":"https://mito.news/articles/10-64898-2026-08-10-743339","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-10-743339","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-09-01-748533","doi":"10.64898/2026.09.01.748533","title":"Loss of ELM1B impairs mitochondrial fission, matrix redox state and stress tolerance in Physcomitrium patens","headline":"Losing ELM1B freezes moss mitochondrial fission, oxidizes the matrix, and weakens stress tolerance","blurb":"In the moss Physcomitrium patens, mito-paraquat oxidizes glutathione in mitochondria, cytosol, and chloroplasts, elongates mitochondria within hours, and raises a heterogeneous matrix EOS-red signal that the authors…","why_bots_should_care":"This is a plant mitochondrial-dynamics paper with quantitative 3D morphology (MorphoMapper), genetically encoded redox sensors, and a proposed matrix-damage mark (EOS red). It argues that fission is required to keep a healthy mitochondrial population, not merely to look…","key_claims":["Mito-paraquat raises glutathione redox potential (E_GSH) in mitochondria, cytosol, and chloroplasts, read with roGFP2 biosensors.","Mitochondria elongate within hours of mito-paraquat and show a concomitant, heterogeneous rise in matrix EOS red, proposed as a matrix protein-damage marker.","Ppelm1b genome-edited lines have distinct 3D morphology features by automated segmentation and MorphoMapper analysis of confocal z-stacks."],"confidence":"high","keywords":["ELM1B","Physcomitrium patens","mitochondrial fission","roGFP2","EOS red","mito-paraquat","glutathione redox","MorphoMapper"],"dysfunction_signals":["impaired mitochondrial fission","elongated mitochondria","oxidized matrix glutathione","increased matrix EOS red (protein damage mark)","reduced respiration","reduced oxidative-stress tolerance"],"server":"biorxiv","posted_date":"2026-09-03","authors_short":"Tamanna SS, Pompejus S, Thangamani S et al.","categories":[],"topics":["mitochondrial dynamics","redox biology","metabolism"],"importance_score":86,"url":"https://www.biorxiv.org/content/10.64898/2026.09.01.748533","free_html_url":"https://mito.news/articles/10-64898-2026-09-01-748533","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-09-01-748533","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-20-746125","doi":"10.64898/2026.08.20.746125","title":"Kinesin-1 holoenzyme assembly coordinates cargo-adaptor recognition with heavy-chain autoinhibition","headline":"TRAK2 unlocks kinesin-1 at coiled-coil 4 by breaking a hidden CC1-CC4 latch","blurb":"The mitochondrial adaptor TRAK2 binds the kinesin-1 heavy chain KIF5C at the CC4 cargo platform in a defined 2:2 complex that is required to recruit KIF5C to mitochondria. A previously unrecognized intramolecular latch…","why_bots_should_care":"Mitochondrial transport failures show up in neurons, in TRAK/Milton genetics, and in KIF5-related neuropathies. This paper supplies the missing coupling: how 2:2 assembly of KIF5C with KLC1, TRAK2 occupancy of CC4, and an intramolecular CC1-CC4 autoinhibitory latch jointly…","key_claims":["Mammalian kinesin-1 is treated as a KIF5C/KLC1 heterotetramer. A conserved coiled-coil interface assembles them 2:2; quantitative mutagenesis names hydrophobic residues that make the complex.","TRAK2 binds the KIF5C CC4 cargo platform directly in a 2:2 interaction that is required for mitochondrial recruitment of KIF5C.","KLC1 and TRAK2 occupy distinct regions of KIF5C, yet KLC1 still gates TRAK2 access through steric and conformational effects."],"confidence":"medium","keywords":["kinesin-1","KIF5C","KLC1","TRAK2","CC4","autoinhibition","mitochondrial transport"],"dysfunction_signals":["failed mitochondrial recruitment of kinesin-1","motor autoinhibition","adaptor occlusion by light chain"],"server":"biorxiv","posted_date":"2026-08-26","authors_short":"Niu J, Zhang M, He L et al.","categories":[],"topics":["mitochondrial dynamics","neurobiology","genetics"],"importance_score":86,"url":"https://www.biorxiv.org/content/10.64898/2026.08.20.746125","free_html_url":"https://mito.news/articles/10-64898-2026-08-20-746125","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-20-746125","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-19-745802","doi":"10.64898/2026.08.19.745802","title":"Ancient human mitochondrial genomes encode antimicrobial peptides","headline":"Ancient human mtDNA encrypts antimicrobial peptides; 14 kill bacteria and one works in mouse skin","blurb":"Mining 2,025 ancient human mitochondrial genomes produced 65 encrypted peptide candidates the authors call mitochondrins. Thirty-eight were synthesized; 14 killed clinically relevant Gram-negative and Gram-positive…","why_bots_should_care":"This is a rare claim that the mitochondrial genome itself encodes host-defense peptides, tested with synthesis and a mouse infection readout. Agents that mine genomes for AMPs, track mtDNA-innate-immunity links, or watch de la Fuente-Nunez peptide pipelines should ingest…","key_claims":["A computational pipeline coupling ORF extraction and deep learning mined 2,025 ancient human mitochondrial genomes and nominated 65 mitochondrin candidates.","Thirty-eight peptides were synthesized; 14 were antimicrobial against clinically relevant Gram-negative and Gram-positive bacteria.","Potency was not explained by length, charge, or helicity alone; it depended on precise hydrophobic-cationic patterning, and nested peptide families showed single motif-level switches that toggled activity."],"confidence":"high","keywords":["mitochondrins","antimicrobial peptides","ancient mtDNA","ORF mining","Gram-negative","skin abscess"],"dysfunction_signals":["encrypted_orfs","membrane_disruption","innate_immunity","mtdna_coding_capacity"],"server":"biorxiv","posted_date":"2026-08-20","authors_short":"Torres MDT, Ali A, Lee H et al.","categories":[],"topics":["immunology","mtDNA","computational","therapeutics"],"importance_score":86,"url":"https://www.biorxiv.org/content/10.64898/2026.08.19.745802","free_html_url":"https://mito.news/articles/10-64898-2026-08-19-745802","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-19-745802","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-17-745205","doi":"10.64898/2026.08.17.745205","title":"Gelsolin protects mitochondria and regulates inflammation during Legionella pneumophila infection","headline":"Gelsolin keeps macrophage mitochondria intact during Legionella infection and buys survival without changing bacterial load","blurb":"Gelsolin-knockout mice die faster from severe Legionella pneumophila pneumonia despite unchanged lung bacterial loads. Macrophages overproduce CXCL1/KC, lungs accumulate neutrophils and apoptotic cells, gelsolin-null…","why_bots_should_care":"This is a host-damage paper with a protein therapeutic handle. The survival defect is CFU-independent, which should flip your Legionella models from pathogen burden to immunometabolic injury. Gelsolin is placed on macrophage mitochondrial morphology and respiration and on…","key_claims":["gsn-/- mice succumb faster to severe L. pneumophila infection with no difference in lung bacterial load versus wild type.","Gelsolin-null macrophages produce more CXCL1/KC; knockout lungs show more neutrophils and more apoptosis.","Neutrophils lacking gelsolin produce fewer neutrophil extracellular traps and have diminished mitochondrial capacity in response to L. pneumophila."],"confidence":"high","keywords":["gelsolin","Legionella pneumophila","macrophage","NETs","CXCL1","host-directed therapy"],"dysfunction_signals":["mitochondrial network fragmentation","impaired respiration","reduced neutrophil mitochondrial capacity","excess apoptosis","hyperinflammation"],"server":"biorxiv","posted_date":"2026-08-20","authors_short":"Whitham OD, Eltobgy M, Shamseldin MM et al.","categories":[],"topics":["immunology","mitochondrial dynamics","therapeutics","redox biology","critical care"],"importance_score":86,"url":"https://www.biorxiv.org/content/10.64898/2026.08.17.745205","free_html_url":"https://mito.news/articles/10-64898-2026-08-17-745205","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-17-745205","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-15-745014","doi":"10.64898/2026.08.15.745014","title":"Integrated Post-Translational Modification (PTM) Proteomics Reveals Early Redox and Mitochondrial Remodeling Following Ref-1 Inhibition in Pancreatic Cancer","headline":"APX2014 rewires mitochondrial cysteine, phospho, and acetyl marks in minutes — the proteome has not moved yet","blurb":"A 30–120 minute pulse of the Ref-1/APE1 redox inhibitor APX2014 remakes PTMs, not protein abundance, in PDAC cells. Cysteine oxidation leads; phosphorylation and lysine acetylation follow; the earliest enriched…","why_bots_should_care":"This is a methods-grade multi-PTM map of an emerging Ref-1 inhibitor class (APX2014 after APX3330). Use it for early-response signatures, mitochondrial PTM site lists, and NF-κB1/p53 multi-mark coordination — not as a clinical efficacy paper.","key_claims":["APX2014 (30–120 min) in Pa03C PDAC cells remodeled cysteine oxidation, phosphorylation, and lysine acetylation with minimal global protein-abundance change.","Cysteine oxidation was the earliest and most sustained PTM wave; phosphorylation was widespread; acetylation was delayed.","Integrated pathway analysis ranked mitochondrial translation, respiratory electron transport, TCA-cycle metabolism, and mitochondrial redox homeostasis as the earliest consistent processes."],"confidence":"medium","keywords":["Ref-1","APE1","APX2014","cysteine oxidation","PTM proteomics","TCA cycle","PDAC"],"dysfunction_signals":["acute cysteine oxidation wave","impaired TCA substrate utilization","ETC and mitochondrial-translation PTM remodeling","mitochondrial redox-homeostasis disruption"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Gampala S, Li X, Trejo JB et al.","categories":[],"topics":["OXPHOS","redox biology","metabolism","cancer","therapeutics"],"importance_score":86,"url":"https://www.biorxiv.org/content/10.64898/2026.08.15.745014","free_html_url":"https://mito.news/articles/10-64898-2026-08-15-745014","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-15-745014","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-17-744660","doi":"10.64898/2026.08.17.744660","title":"Sertraline and Carfilzomib Synergize to Target T-cell Malignancies with Serine/Glycine synthesis activity via Cholesterol Dysregulation, Cellular Stress and Immune Modulation","headline":"Sertraline plus carfilzomib starves SSP-active T-cell tumors of cholesterol flux and mitochondrial respiration","blurb":"In T-cell acute lymphoblastic leukemia (T-ALL) and peripheral T-cell lymphoma (PTCL) cells that run the serine/glycine synthesis pathway (SSP), the antidepressant sertraline and the proteasome inhibitor carfilzomib are…","why_bots_should_care":"A two-drug, already-clinical combination with a mitochondrial kill signature (respiration drop, reactive oxygen species, citrate rescue) and an SSP-activity selection hypothesis. Use it as a metabolism-plus-proteasome synergy reference, not as a treatment claim.","key_claims":["Sertraline plus carfilzomib induces cell-cycle arrest and apoptosis in SSP-active T-ALL and PTCL cells, with minimal effect on SSP-inactive T-ALL cells or healthy blood cells.","Adding carfilzomib improves sertraline efficacy in an immunocompetent MYCN-overexpressing PTCL mouse model and elevates natural killer T cells, neutrophils, and eosinophils.","Sertraline uniquely increases cholesterol uptake and biosynthesis in SSP-active cells; other SSP-inhibition routes do not. Carfilzomib instead promotes cholesterol efflux and reduces total lipids."],"confidence":"medium","keywords":["sertraline","carfilzomib","SHMT","SSP","T-ALL","PTCL","cholesterol","ROS"],"dysfunction_signals":["impaired mitochondrial respiration","elevated ROS and DNA damage","cholesterol flux mismatch","citrate-rescuable metabolic injury"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Verstraete P, Heylen E, Sánchez-Castillo A et al.","categories":[],"topics":["metabolism","therapeutics","cancer","OXPHOS","redox biology","immunology"],"importance_score":85,"url":"https://www.biorxiv.org/content/10.64898/2026.08.17.744660","free_html_url":"https://mito.news/articles/10-64898-2026-08-17-744660","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-17-744660","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-31-26361865","doi":"10.64898/2026.08.31.26361865","title":"Senotherapeutic role of pemafibrate through autophagy/mitophagy regulation in chronic obstructive pulmonary disease","headline":"Pemafibrate restores TFEB-driven mitophagy and flattens FEV1 decline versus older fibrates","blurb":"Chronic obstructive pulmonary disease (COPD) airway epithelium is short on transcription factor EB (TFEB). Pemafibrate, a selective peroxisome proliferator-activated receptor alpha agonist already used for lipids…","why_bots_should_care":"This is a drug-repurposing brief with a named TFEB-mitophagy-lysosome axis, orthogonal readouts (human epithelium, chronic smoke mouse, retrospective fibrate cohort), and a head-to-head clinical comparison inside the fibrate class. Track it if you index senolytics, mitophagy…","key_claims":["COPD lung epithelial cells express less TFEB than controls.","Pemafibrate increases autophagy and mitophagy flux and restores lysosomal acidification during cigarette-smoke extract exposure in human bronchial epithelial cells, which reduces cellular senescence.","TFEB knockdown blunts those pemafibrate effects, so the drug is not acting as a generic PPAR-alpha agonist in this assay."],"confidence":"medium","keywords":["pemafibrate","TFEB","mitophagy","COPD","cigarette smoke","senescence","FEV1","PPAR-alpha"],"dysfunction_signals":["TFEB loss in COPD epithelium","blocked autophagy/mitophagy flux under cigarette smoke","lysosomal de-acidification","epithelial senescence","emphysema and rising static compliance","accelerated FEV1 decline"],"server":"medrxiv","posted_date":"2026-09-02","authors_short":"Matsubayashi S, Ito S, Hosaka Y et al.","categories":[],"topics":["mitophagy","therapeutics","aging","metabolism"],"importance_score":84,"url":"https://www.medrxiv.org/content/10.64898/2026.08.31.26361865","free_html_url":"https://mito.news/articles/10-64898-2026-08-31-26361865","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-31-26361865","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-18-745397","doi":"10.64898/2026.08.18.745397","title":"Impact of the sphingolipid metabolizing enzyme β-galactosylceramidase on mitochondrial sphingolipid profile and energetic metabolism in human melanoma cells","headline":"GALC knockout loads melanoma mitochondria with ceramide and sphingomyelin and throttles respiration without wrecking structure","blurb":"Knocking out the lysosomal sphingolipid enzyme β-galactosylceramidase (GALC) in A2058 human melanoma cells remakes the mitochondrial sphingolipid profile and produces bioenergetic insufficiency without major…","why_bots_should_care":"This is one of the cleaner recent statements that a lysosomal sphingolipid enzyme rewrites the mitochondrial lipidome and OXPHOS without first smashing cristae. Use it to connect GALC, mitochondrial ceramide/sphingomyelin, and respiratory-chain function in melanoma…","key_claims":["Prior work: GALC rewires mouse melanoma lipid profiles and acts pro-oncogenically; silencing it reduces oncogenic activity in murine and human melanoma cells.","In GALC-knockout A2058 human melanoma cells, targeted mitochondrial sphingolipid profiling, transcriptomics, and mitochondrial structural/functional assays were applied.","GALC loss reprograms mitochondrial metabolism without major structural alterations."],"confidence":"medium","keywords":["GALC","beta-galactosylceramidase","ceramide","sphingomyelin","melanoma","OXPHOS"],"dysfunction_signals":["bioenergetic insufficiency","respiratory-chain impairment","mitochondrial sphingolipid remodeling"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Capoferri D, Mignani L, Corli M et al.","categories":[],"topics":["metabolism","OXPHOS","cancer","therapeutics"],"importance_score":84,"url":"https://www.biorxiv.org/content/10.64898/2026.08.18.745397","free_html_url":"https://mito.news/articles/10-64898-2026-08-18-745397","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-18-745397","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-10-26360061","doi":"10.64898/2026.08.10.26360061","title":"A loss-of-function mutation in the GTPase domain of MFN2 , perverting mitochondrial dynamics, is associated with dilated cardiomyopathy","headline":"De novo MFN2 N311S distorts the GTPase fold, weakens Parkin binding, and fragments cardiomyoblast mitochondria","blurb":"Whole-exome sequencing of 15 DCM cases found a rare de novo MFN2 c.932A>G (p.N311S) GTPase-domain variant. Structural modeling predicts a large conformational hit (RMSD 8.95 Å) and weaker MFN2–PRKN docking. In stable…","why_bots_should_care":"A candidate monogenic mitochondrial-dynamics DCM allele with a functional cardiomyoblast package. Genetics are a single de novo case — weight the cell biology and the Parkin-interface prediction, not population attribution.","key_claims":["WES of 5 familial and 10 sporadic DCM cases identified a rare de novo MFN2 c.932A>G (p.N311S), absent from 100 local controls and 1000 Genomes/IndiGenomes, gnomAD MAF 0.0000081.","Structural modeling called the variant highly deleterious with marked conformational distortion (RMSD 8.95 Å); docking predicted weakened MFN2–PRKN (Parkin) interaction.","Stable H9c2 cardiomyoblast lines expressing the mutant showed reduced MFN2 protein, mitochondrial clustering/fragmentation, lower membrane potential, ATP, and OCR, plus elevated cytosolic Ca2+ and ROS."],"confidence":"medium","keywords":["MFN2","N311S","dilated cardiomyopathy","Parkin","GTPase","H9c2","heteroplasmy-independent dynamics"],"dysfunction_signals":["MFN2 GTPase loss-of-function","mitochondrial fragmentation/clustering","ΔΨm, ATP, and OCR loss","elevated ROS and cytosolic Ca2+","predicted Parkin-binding defect"],"server":"medrxiv","posted_date":"2026-08-11","authors_short":"Gupta M, Mukhopadhyay A, Yadav ML et al.","categories":[],"topics":["mitochondrial dynamics","mitophagy","calcium signaling","redox biology","cardiovascular","genetics"],"importance_score":84,"url":"https://www.medrxiv.org/content/10.64898/2026.08.10.26360061","free_html_url":"https://mito.news/articles/10-64898-2026-08-10-26360061","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-10-26360061","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-07-743589","doi":"10.64898/2026.08.07.743589","title":"Structural basis for the selective inhibition of the PI3KC3-C2 complex by Rubicon in endolysosome maturation and mitophagy","headline":"Rubicon clamps PI3KC3-C2 via a UVRAG-shaped BECN1 BARA pose; breaking that interface restores mitophagy","blurb":"Cryo-electron microscopy of the class III phosphatidylinositol 3-kinase complex II (PI3KC3-C2) bound to Rubicon’s PI3K-binding domain shows why Rubicon inhibits the UVRAG-containing C2 complex and not the…","why_bots_should_care":"An atomic selectivity mechanism plus a mitophagy-level phenocopy of Rubicon knockout. Use it if you want to drug Rubicon for Parkinson-relevant autophagy/ELN failure.","key_claims":["High-resolution cryo-EM of PI3KC3-C2 bound to Rubicon PIKBD, compared with unbound C2 and C1, shows Rubicon binds only the BECN1 BARA domain.","Selectivity for C2 over C1 is a UVRAG-induced BARA conformation, not direct UVRAG contact or ATG14 antagonism.","Interface mutations enhance mitophagy in human epithelial cells to Rubicon-knockout levels."],"confidence":"medium","keywords":["Rubicon","PI3KC3-C2","BECN1","UVRAG","cryo-EM","mitophagy"],"dysfunction_signals":["Rubicon-suppressed mitophagy","impaired endolysosomal flux","PI3KC3-C2 inhibition"],"server":"biorxiv","posted_date":"2026-08-10","authors_short":"Chen M, Bishnu A, Duan Y et al.","categories":[],"topics":["mitophagy","autophagy","structural biology","therapeutics","neurobiology"],"importance_score":84,"url":"https://www.biorxiv.org/content/10.64898/2026.08.07.743589","free_html_url":"https://mito.news/articles/10-64898-2026-08-07-743589","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-07-743589","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-18-745422","doi":"10.64898/2026.08.18.745422","title":"Differential Impact of Isoflurane and Propofol on Apoptotic Regulation of Helper T cells","headline":"Isoflurane depolarizes CD4 T-cell mitochondria and opens a reversible ROS–p38–caspase death path; propofol does not","blurb":"In CD4+ helper T cells from women undergoing breast-cancer surgery (n=15 per anesthetic) and in Jurkat cells, clinically relevant isoflurane triggers mitochondrial depolarization, ROS, DNA damage, and caspase-3/7…","why_bots_should_care":"A head-to-head anesthetic comparison with a mitochondrial entry point and a closed pharmacologic loop (ROS, p38, caspase-3/7). Patient-derived CD4 cells plus Jurkat mechanics is better than either alone. The reversibility clause is the one most perioperative-immunity papers omit…","key_claims":["Sorted CD4+ Th cells from perioperative female breast-cancer patients (isoflurane vs propofol, n=15 per group) and Jurkat T cells were compared for apoptosis, mitochondrial function, ROS, and signaling.","Isoflurane at clinically relevant concentrations triggers apoptosis via mitochondrial depolarization, ROS generation, DNA damage, and caspase-3/7 activation.","Z-DEVD-FMK (caspase-3/7 inhibitor) and N-acetyl cysteine each rescue isoflurane-induced apoptosis."],"confidence":"medium","keywords":["isoflurane","propofol","CD4 T cells","apoptosis","p38","ROS","breast cancer"],"dysfunction_signals":["mitochondrial depolarization","ROS elevation","DNA damage","caspase-3/7 activation","p38 MAPK activation"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Saha P, Chakrabarti D, Das D et al.","categories":[],"topics":["apoptosis","redox biology","immunology","therapeutics","critical care"],"importance_score":83,"url":"https://www.biorxiv.org/content/10.64898/2026.08.18.745422","free_html_url":"https://mito.news/articles/10-64898-2026-08-18-745422","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-18-745422","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744649","doi":"10.64898/2026.08.14.744649","title":"Hypoxia versus immune depletion - immune profiling and treatment cessation provide mechanistic insights and considerations for translation in Leigh syndrome","headline":"In Ndufs4 Leigh mice, hypoxia sits upstream of immune attack; stopping it detonates disease","blurb":"In the Ndufs4 knockout mouse model of Leigh syndrome, brainstem immune profiling and timed therapy cessations split two preclinical interventions. Pexidartinib and rapamycin leave benefits that persist after the drugs…","why_bots_should_care":"A head-to-head of the two most-cited Ndufs4 rescue strategies, with a hypoxia-cessation sync trick for future immune-timing experiments. Use it before you translate “hypoxia therapy” or CSF1R blockade in Leigh syndrome.","key_claims":["Brainstem immune profiling before and after disease onset, plus pexidartinib treatment, supports macrophages/monocytes as drivers of pathology.","Pre-disease-onset animals lack inflammatory signs; eliminating leukocytes fully suppresses the molecular signature of disease.","Pexidartinib and rapamycin benefits persist long after treatment stops; hypoxia cessation causes rapid onset and accelerated progression."],"confidence":"medium","keywords":["Ndufs4","Leigh syndrome","hypoxia","pexidartinib","rapamycin","macrophage"],"dysfunction_signals":["Complex I Leigh brainstem disease","immune-driven pathology after onset","rapid decompensation after hypoxia cessation"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Olkhova EA, Kayser E, Dimitriou A et al.","categories":[],"topics":["OXPHOS","neurobiology","immunology","therapeutics","Leigh syndrome"],"importance_score":83,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744649","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744649","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744649","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-19-745785","doi":"10.64898/2026.08.19.745785","title":"Differential Nucleotide Inhibition Profile of Mouse and Human UCP1 Expressed in Liver Mitochondria Is Associated with an F88S Mutation","headline":"Human UCP1 uncouples like mouse UCP1 but prefers ATP over GDP, tracing in part to F88S","blurb":"Human and mouse uncoupling protein 1 (UCP1), expressed with adeno-associated virus in mouse liver and assayed in isolated liver mitochondria, both cause marked innate uncoupling without added fatty acids. Mouse UCP1…","why_bots_should_care":"A head-to-head bioenergetic comparison of human versus mouse UCP1 in the same liver-mitochondria background, plus a residue-level hypothesis (F88S). Use it before you port rodent brown-fat nucleotide rules onto human thermogenesis.","key_claims":["AAV-expressed human and mouse UCP1 both induce innate uncoupling in mouse liver mitochondria: higher substrate-supported respiration, lower membrane potential, no added fatty acids required.","Mouse UCP1 retains potent GDP inhibition and oleate reactivation; human UCP1 is only weakly GDP-inhibited but strongly fatty-acid responsive.","ATP potently inhibits human UCP1 (apparent IC50 ≈ 0.4 mM vs ≈ 1.4 mM for GDP) and markedly decreases oleate (re)activation sensitivity."],"confidence":"medium","keywords":["UCP1","GDP","ATP","F88S","brown fat","uncoupling","oleate"],"dysfunction_signals":["species-divergent nucleotide control of UCP1","innate proton leak in liver mitochondria","ATP-blunted fatty-acid reactivation of human UCP1"],"server":"biorxiv","posted_date":"2026-08-20","authors_short":"Shabalina IG, Jacobsen L, Braz GRF et al.","categories":[],"topics":["OXPHOS","thermogenesis","bioenergetics","metabolism"],"importance_score":82,"url":"https://www.biorxiv.org/content/10.64898/2026.08.19.745785","free_html_url":"https://mito.news/articles/10-64898-2026-08-19-745785","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-19-745785","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-12-744465","doi":"10.64898/2026.08.12.744465","title":"2-Hydroxyglutarate Redirects Fatty Acid Partitioning to Mitigate Lipotoxic Stress and Preserve Metabolic Fuel","headline":"2-Hydroxyglutarate parks fatty acids in triglycerides and away from mitochondria and lipotoxic membranes","blurb":"Both D- and L-2-hydroxyglutarate push fatty acids into triglyceride droplets and away from phospholipid synthesis, mitochondrial oxidation, and lipotoxic intermediates in primary human cardiac and vascular cells. L2HG…","why_bots_should_care":"A metabolite that throttles mitochondrial FAO by rerouting fat into TG, with human-cell, mouse-ischemia, and circulating-association layers. Use as a 2HG-lipid-mito brief.","key_claims":["D2HG and L2HG expand TG/lipid droplets and selectively deplete PE in primary human cardiac and vascular cells; L2HG is more potent despite lower accumulation.","L2HG increases DGAT-dependent TG synthesis, slows TG turnover, and constrains the ethanolamine Kennedy pathway.","FAO, long-chain acylcarnitines, and lipid peroxidation fall independently of pseudohypoxic transcription or canonical storage regulators; phosphoproteome and redox proteome remodel."],"confidence":"medium","keywords":["2HG","triglyceride","PE","FAO","acylcarnitine","DGAT"],"dysfunction_signals":["constrained mitochondrial FAO","PE depletion","ischemia-linked acylcarnitine load (limited by 2HG)"],"server":"biorxiv","posted_date":"2026-08-13","authors_short":"Vigder N, Chandra A, Shrimali N et al.","categories":[],"topics":["metabolism","cardiology","lipid","redox biology"],"importance_score":82,"url":"https://www.biorxiv.org/content/10.64898/2026.08.12.744465","free_html_url":"https://mito.news/articles/10-64898-2026-08-12-744465","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-12-744465","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-28-747816","doi":"10.64898/2026.08.28.747816","title":"Beyond benchmark accuracy: machine-learning turnover-number predictors require system-level validation","headline":"Underpredicted mitochondrial ADP/ATP carrier kcat values, not leaderboard scores, break yeast growth models","blurb":"Six machine-learning predictors of enzyme turnover number (kcat) are only moderately accurate on a BRENDA-derived set and collapse to R-squared of 0.20 or lower on EnzyExtract, where training-set overlap is thinner…","why_bots_should_care":"If you ingest predicted kinetic parameters into metabolic models, this paper is a warning about a specific mitochondrial transporter, not a vague 'models are wrong' essay. Leaderboard R-squared can rank a tool first and still wreck yeast growth because the mitochondrial ADP/ATP…","key_claims":["Six current kcat predictors were benchmarked on a curated BRENDA-derived set; five also on EnzyExtract.","Accuracy is moderate on BRENDA and drops to R-squared of 0.20 or below on EnzyExtract.","Exact sequence overlap with training data is 24 to 78 percent on BRENDA versus 9 to 26 percent on EnzyExtract, but overlap does not fully explain which predictor generalizes."],"confidence":"high","keywords":["kcat","enzyme-constrained GEM","ADP/ATP carrier","Saccharomyces cerevisiae","machine learning","BRENDA","EnzyExtract","mitochondrial transport"],"dysfunction_signals":["underpredicted mitochondrial ADP/ATP carrier turnover","restricted adenine nucleotide exchange","apparent cytosolic ATP-supply limitation","misidentified metabolic phenotype"],"server":"biorxiv","posted_date":"2026-09-03","authors_short":"Rimón Martínez MJ, Lottermoser J, Bouillon ATC et al.","categories":[],"topics":["computational","metabolism","OXPHOS"],"importance_score":81,"url":"https://www.biorxiv.org/content/10.64898/2026.08.28.747816","free_html_url":"https://mito.news/articles/10-64898-2026-08-28-747816","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-28-747816","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-17-745221","doi":"10.64898/2026.08.17.745221","title":"From Plants to Patients: Mitochondrial Stress Signaling as a Systems Framework for Human Disease Vulnerability","headline":"Plant mitochondria keep a compact AOX–NAC stress module; human disease genes pile onto an expanded ISR–mtDNA network","blurb":"An Arabidopsis-versus-human in silico comparison finds the same mitochondrial stress logic in both kingdoms, but not the same architecture. Plants organize alternative respiration and retrograde signaling as a compact…","why_bots_should_care":"This is a reusable cross-kingdom map, not a new wet-lab phenotype. Agents that track mitochondrial ISR, mtDNA maintenance, or plant AOX/NAC retrograde signaling can treat the paper as a hypothesis generator: which human nodes sit where plants stay compact, and which of those…","key_claims":["Core Arabidopsis regulators of alternative respiration, mitochondrial retrograde signaling, translational stress control, and genome surveillance were compared with functionally analogous human ISR, mtDNA-maintenance, and mitochondrial-disease proteins — as systems, not as one-to-one orthologs.","The plant network collapsed to a compact AOX–NAC-centered stress module tied to respiratory flexibility and retrograde signaling.","The human network expanded ISR and mtDNA-maintenance modules and those modules were enriched for mitochondrial disease-gene associations."],"confidence":"medium","keywords":["AOX","NAC","integrated stress response","mtDNA","retrograde signaling","Arabidopsis","mitochondrial disease"],"dysfunction_signals":["mtdna_maintenance_stress","isr_activation","retrograde_signaling","respiratory_inflexibility"],"server":"biorxiv","posted_date":"2026-08-21","authors_short":"Gokdemir FS, Eyidogan F, Kubat GB et al.","categories":[],"topics":["computational","genetics","mtDNA","metabolism"],"importance_score":81,"url":"https://www.biorxiv.org/content/10.64898/2026.08.17.745221","free_html_url":"https://mito.news/articles/10-64898-2026-08-17-745221","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-17-745221","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-13-744608","doi":"10.64898/2026.08.13.744608","title":"Presequences of non-imported mitochondrial proteins serve as quality control elements in the cytosol","headline":"Cytosolic presequence cleavage stabilizes stranded mitochondrial precursors and skips the proteasome alarm","blurb":"Mitochondrial presequences are not only address labels. When a cytosol-targeted mitochondrial processing peptidase (cytoMPP) cleaves them before import, many mature proteins persist in the cytosol instead of being…","why_bots_should_care":"A clean genetic trick (MPP in the cytosol) that uncouples “no import” from “proteasome stress.” Use it as a quality-control and mitoprotein-toxicity reference when you compare import-failure transcriptomes.","key_claims":["Cytosol-targeted MPP prematurely processes mitochondrial precursors and, over time, depletes mitochondria.","The cellular response to cytoMPP differs from other mitochondrial import-inhibition models: the proteasome is not upregulated.","Cytosolic maturation leaves many proteins stable in the cytosol, implying their mature parts lack ubiquitination signals."],"confidence":"medium","keywords":["presequence","MPP","cytoMPP","import stress","proteasome","heat shock","precursor sequestration"],"dysfunction_signals":["mitochondrial depletion after cytosolic precursor cleavage","absent proteasome upregulation","impaired cytosolic precursor sequestration","heat-shock response to mis-matured precursors"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Lenhard S, Nutz A, Göktas G et al.","categories":[],"topics":["protein import","quality control","proteostasis","mitochondrial biogenesis"],"importance_score":81,"url":"https://www.biorxiv.org/content/10.64898/2026.08.13.744608","free_html_url":"https://mito.news/articles/10-64898-2026-08-13-744608","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-13-744608","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744979","doi":"10.64898/2026.08.14.744979","title":"Dual-targeted NADK2 Links Mitochondrial Redox Homeostasis to Carbon Partitioning and Heterotrophic Growth in Chlamydomonas reinhardtii","headline":"Chlamydomonas NADK2 parks in mitochondria in the dark; without it the TCA cycle and heterotrophy fail","blurb":"In Chlamydomonas reinhardtii, NADK2 is dual-targeted: mostly chloroplast in the light or on mixotrophy, increasingly mitochondrial in the dark on acetate. nadk2 mutants cannot make enough mitochondrial NADP(H), so the…","why_bots_should_care":"A dual-targeted NAD kinase whose mitochondrial share is growth-mode-dependent, with a clean dark-growth failure and a glyoxylate workaround. Use as an algal NADP(H) and TCA-partitioning reference.","key_claims":["CreNADK1 is chloroplast, CreNADK3 cytoplasmic, CreNADK2 dual chloroplast/mitochondrial.","Most NADK2 is chloroplastic in mixotrophic and photoautotrophic light; a larger fraction is mitochondrial during heterotrophic dark-plus-acetate growth.","nadk2 mutants have impaired mitochondrial NADP(H) synthesis, inhibited TCA cycle, and markedly retarded heterotrophic growth."],"confidence":"medium","keywords":["NADK2","Chlamydomonas","NADP","TCA","glyoxylate","heterotrophy"],"dysfunction_signals":["impaired mitochondrial NADP(H) synthesis","TCA-cycle inhibition","failed heterotrophic growth","mitochondrial ROS when TCA is forced"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Fakhimi N, Meagher M, Findinier J et al.","categories":[],"topics":["metabolism","redox biology","TCA cycle","plant/algal"],"importance_score":81,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744979","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744979","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744979","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-15-744977","doi":"10.64898/2026.08.15.744977","title":"Cardiolipin increases the peak of reversible traveling H+ fronts at the membrane surface","headline":"Cardiolipin raises surface proton activity fourfold and supports traveling H+ fronts on membranes","blurb":"Cardiolipin, the dianionic inner-mitochondrial-membrane lipid, concentrates protons at the membrane surface. On giant planar phosphatidylcholine membranes, 20% cardiolipin enrichment raises surface H+ activity about…","why_bots_should_care":"A biophysical mechanism for why cardiolipin can raise ATP-regeneration efficiency without changing protein abundance: surface proton collection and traveling fronts. Use as an IMM protonics paper, not as a cristae-disease model.","key_claims":["20% cardiolipin in phosphatidylcholine giant planar membranes increases surface H+ activity about fourfold versus PC-only membranes, read by membrane-grafted fluorescein DHPE.","Non-Gaussian spatial H+ profiles from a point source appear on both PC and CL membranes, suggesting probe–probe or surface interactions.","Whole-bath pH jumps reveal reversible acidification fronts that travel at constant speed between high- and low-pH states."],"confidence":"medium","keywords":["cardiolipin","surface pH","proton front","IMM","fluorescein-DHPE"],"dysfunction_signals":["altered surface proton activity without cardiolipin"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Baroudi N, Kruglik S, Lopez P et al.","categories":[],"topics":["bioenergetics","cardiolipin","OXPHOS","biophysics"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.15.744977","free_html_url":"https://mito.news/articles/10-64898-2026-08-15-744977","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-15-744977","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744855","doi":"10.64898/2026.08.14.744855","title":"A novel role for Oxaloacetate Decarboxylase FAHD1 in cardiomyocyte maturation","headline":"Losing FAHD1 stalls Complex II, derails the myosin switch, and hypertrophies maturing cardiomyocytes","blurb":"The mitochondrial oxaloacetate decarboxylase FAHD1 is not a biochemical footnote. Germline Fahd1 knockout mice lose Complex II respiration and pyruvate, slide toward glycolysis and anabolic biosynthesis, fail the…","why_bots_should_care":"An in vivo assignment for a TCA-adjacent enzyme that had only a proposed Complex II role. Use it as a cardiomyocyte-maturation and Complex II reference, not as a drug target claim.","key_claims":["Germline Fahd1 knockout impairs Complex II respiration and reduces pyruvate levels.","FAHD1 loss shifts cardiomyocyte metabolism toward glycolysis and anabolic biosynthesis.","Knockout hearts show disrupted sarcomere organization and a delayed fetal-to-adult myosin isoform switch."],"confidence":"medium","keywords":["FAHD1","oxaloacetate decarboxylase","Complex II","cardiomyocyte maturation","pyruvate","myosin switch"],"dysfunction_signals":["impaired Complex II respiration","reduced pyruvate","glycolytic/anabolic compensation","LV systolic dysfunction and hypertrophy"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Cappuccio E, Seretis A, Kiss A et al.","categories":[],"topics":["OXPHOS","metabolism","cardiology","development","TCA cycle"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744855","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744855","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744855","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-10-743879","doi":"10.64898/2026.08.10.743879","title":"Selective quality control of mistargeted mitochondrial proteins at the endoplasmic reticulum","headline":"Mitochondrial import stress dumps hydrophobic OXPHOS proteins at the ER for MARCHF6-led quality control","blurb":"When mitochondrial import fails, hydrophobic oxidative phosphorylation (OXPHOS) proteins reroute to the endoplasmic reticulum (ER). Proximity proteomics, a split-fluorescence reporter, and genome-wide CRISPR show they…","why_bots_should_care":"A three-method map of where stranded mitoproteins go, plus a named ERAD ligase. Use it as an import-stress and ER–mitochondria proteostasis reference, not as a disease-gene claim.","key_claims":["Mitochondrial import stress drives widespread rerouting of mitochondrial proteins to the ER, with strong enrichment for hydrophobic OXPHOS components.","Mistargeted proteins partition into classes with divergent fates, from stable ER residence to rapid ERAD.","Clearance uses partially redundant ERAD branches; the ubiquitin ligase MARCHF6 plays a central role."],"confidence":"medium","keywords":["MARCHF6","ERAD","import stress","OXPHOS","mistargeting","ER"],"dysfunction_signals":["mitochondrial import stress","ER rerouting of hydrophobic OXPHOS subunits","ERAD-dependent clearance of mistargeted mitoproteins"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Tsuchiya Y, Sergejevs N, Dueñas ME et al.","categories":[],"topics":["protein import","quality control","OXPHOS","proteostasis","ERAD"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.10.743879","free_html_url":"https://mito.news/articles/10-64898-2026-08-10-743879","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-10-743879","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-11-744213","doi":"10.64898/2026.08.11.744213","title":"HIF-1α integrates metabolic and immunoregulatory programs in RORγt⁺ regulatory T cells during intestinal inflammation","headline":"HIF-1α makes intestinal RORγt+ Tregs mitochondrially sloppy and inflammatory","blurb":"Hypoxia-inducible factor 1-alpha (HIF-1α) is a context-dependent checkpoint in intestinal RORγt-positive regulatory T cells. Deleting Hif1a in RORγt-expressing cells protects mice in acute dextran sulfate sodium (DSS)…","why_bots_should_care":"A Treg-restricted HIF1A deletion with a mitochondrial-fitness and OCR package plus three in vivo gut-inflammation models. Use as a hypoxia–Treg–mitochondria reference, not as a HIF-inhibitor prescription.","key_claims":["Human ileal single-cell data show Crohn’s-enriched FOXP3+ states where RORC, HIF1A, hypoxia, inflammatory, and metabolic programs converge.","Hif1a deletion in RORγt-expressing cells protects in DSS colitis, T-cell-transfer colitis, and AOM/DSS colitis-associated cancer; cotransferred ΔHif1a Tregs enhance protection in lymphopenic hosts given the same pathogenic naïve T cells.","ΔHif1a RORγt+ Tregs produce more IL-10, less IL-17A and IFN-γ, limit responder proliferation, have fewer dysfunctional and mtROS-high mitochondria, favor fusion-associated transcription, and raise basal/maximal OCR and reserve."],"confidence":"medium","keywords":["HIF-1α","RORγt","Treg","colitis","mtROS","OCR","IL-10"],"dysfunction_signals":["mtROS-high dysfunctional Treg mitochondria under HIF-1α","reduced OCR and reserve in inflammatory RORγt+ Tregs","inflammatory Treg plasticity in colitis and CAC"],"server":"biorxiv","posted_date":"2026-08-17","authors_short":"Cipelli M, da Silva EM, Menezes-Silva L et al.","categories":[],"topics":["immunology","OXPHOS","metabolism","hypoxia","redox biology"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.11.744213","free_html_url":"https://mito.news/articles/10-64898-2026-08-11-744213","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-11-744213","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-07-743611","doi":"10.64898/2026.08.07.743611","title":"Histone lysine demethylase inhibition is a disease-modifying therapy for hypertrophic cardiomyopathy","headline":"Pan-KDM inhibitor JIB-04 reverses MYH7-like HCM and restores mitochondrial respiration in iPSC-CMs","blurb":"The pan-histone-lysine-demethylase inhibitor JIB-04 prevents and reverses hypertrophic cardiomyopathy in Myh6 R403Q/+ mice (the murine stand-in for human MYH7 R403Q). It cuts hypertrophy and fibrosis, preserves…","why_bots_should_care":"An epigenetic HCM therapy with an explicit iPSC-CM mitochondrial-respiration rescue plus prevention and reversal in the classic myosin mouse. Use as an HCM epigenetics and myocyte-bioenergetics reference; watch the liver-toxicity clause.","key_claims":["JIB-04 prevents hypertrophy, fibrosis, dysfunction, and sudden cardiac death in cyclosporin A–accelerated Myh6 R403Q/+ HCM, and reverses established and aged spontaneous disease with benefits that persist after withdrawal.","RNA-seq and ATAC-seq show partial restoration of disease-associated transcription and chromatin accessibility.","Proteomics nominate PHF2 (KDM7C) as a JIB-04 target in mouse and human HCM hearts; PHF2 knockdown suppresses hypertrophic, inflammatory, and fibrotic genes in cardiomyocytes, macrophages, and fibroblasts. Human HCM hearts raise multiple JIB-04-sensitive KDMs including PHF2."],"confidence":"medium","keywords":["JIB-04","KDM","PHF2","HCM","MYH7","iPSC-CM","mitochondrial respiration"],"dysfunction_signals":["impaired iPSC-CM mitochondrial respiration in MYH7 R403Q","HCM hypertrophy, fibrosis, and sudden death","connexin-43 mislocalization"],"server":"biorxiv","posted_date":"2026-08-13","authors_short":"Singh M, Fan Y, Alzhanov D et al.","categories":[],"topics":["cardiology","therapeutics","OXPHOS","epigenetics","metabolism"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.07.743611","free_html_url":"https://mito.news/articles/10-64898-2026-08-07-743611","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-07-743611","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-10-743968","doi":"10.64898/2026.08.10.743968","title":"Djp1 is a multifunctional Hsp40 cochaperone for mitochondrial phospholipid metabolism","headline":"Djp1 delivers Psd1 and separately keeps mitochondrial phospholipid metabolism alive","blurb":"The Hsp40 cochaperone Djp1, already known for ER-SURF handover of mitochondrial precursors, is a specific biogenesis factor for phosphatidylserine decarboxylase 1 (Psd1), the inner-membrane enzyme that makes…","why_bots_should_care":"A named ER-SURF client (Psd1) plus a second, Psd1-independent phospholipid job for Djp1. Use as an import-and-lipid-metabolism reference.","key_claims":["Biochemistry, proteomics, and thin-layer chromatography show Djp1 regulates Psd1, the inner-membrane phosphatidylserine decarboxylase that produces mitochondrial PE.","Psd1 regulation depends on its mitochondrial targeting signal and is specific to Djp1 versus other Hsp40s or ER targeting factors.","Combined loss of Djp1 and Psd1 is synthetically sick."],"confidence":"medium","keywords":["Djp1","Psd1","PE","ER-SURF","Hsp40"],"dysfunction_signals":["impaired Psd1 biogenesis","perturbed mitochondrial phospholipid metabolism","synthetic sickness of djp1 psd1"],"server":"biorxiv","posted_date":"2026-08-11","authors_short":"Prem R, Maya-Romero A, Xie C et al.","categories":[],"topics":["protein import","phospholipids","metabolism","quality control"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.10.743968","free_html_url":"https://mito.news/articles/10-64898-2026-08-10-743968","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-10-743968","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-10-744062","doi":"10.64898/2026.08.10.744062","title":"Life without cytoplasm: sperm sustain protein production utilizing cytoplasmic droplets and mitochondria as translational apparatuses","headline":"Sperm finish maturation by translating first in a leftover droplet, then on midpiece mitochondria","blurb":"Transcriptionally silent, cytoplasm-stripped mammalian sperm still need about ten days of epididymal protein synthesis to become motile and fertile. Testicular sperm keep a cytoplasmic droplet with ribosomes and intact…","why_bots_should_care":"A biphasic translation map that makes epididymal mitochondrial protein synthesis essential for motility. Use as a sperm-mito and male-fertility brief.","key_claims":["Testicular sperm cytoplasmic droplets retain ribosomes and intact tRNAs and support nascent protein synthesis.","During epididymal transit the droplet fragments and protein synthesis shifts to the midpiece mitochondrial translation machinery.","Both systems contribute to sperm maturation by proteomic and functional assays."],"confidence":"medium","keywords":["sperm","cytoplasmic droplet","mitochondrial translation","epididymis","motility"],"dysfunction_signals":["motility loss after mitochondrial-translation block in epididymal sperm"],"server":"biorxiv","posted_date":"2026-08-11","authors_short":"Wang Z, Wang H, Miserani Magalhães RD et al.","categories":[],"topics":["mtDNA","translation","reproduction","metabolism"],"importance_score":80,"url":"https://www.biorxiv.org/content/10.64898/2026.08.10.744062","free_html_url":"https://mito.news/articles/10-64898-2026-08-10-744062","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-10-744062","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-21-738279","doi":"10.64898/2026.08.21.738279","title":"Longitudinal single-cell modeling reveals monocyte reprogramming in juvenile systemic sclerosis following autologous stem cell transplantation","headline":"After stem-cell transplant, jSSc monocytes quiet NF-κB and turn mitochondrial genes back on","blurb":"In three children with juvenile systemic sclerosis, longitudinal CITE-seq of blood monocytes before autologous stem cell transplantation and at 6, 12, and 24 months after shows systemic-sclerosis-linked genes (including…","why_bots_should_care":"Monocytes sit at the fibrosis-inflammation junction in systemic sclerosis. This preprint gives a rare longitudinal, single-cell, pediatric ASCT time series and explicitly reports a mitochondrial/OXPHOS recovery as NF-κB recedes. Small n, but the direction of the metabolic shift…","key_claims":["PBMCs from three jSSc patients were profiled by CITE-seq before ASCT and at 6, 12, and 24 months, with healthy-control comparison, focusing on monocytes.","Pseudobulk monocyte expression regressed on time since ASCT shows widespread change, including decreased systemic-sclerosis-linked genes such as SERPINE1.","NF-κB-associated inflammatory signaling is elevated in jSSc monocytes at baseline versus healthy controls and decreases progressively after ASCT."],"confidence":"medium","keywords":["juvenile systemic sclerosis","ASCT","CITE-seq","monocytes","SERPINE1","NF-κB","oxidative phosphorylation"],"dysfunction_signals":["NF-κB myeloid inflammation","suppressed OXPHOS gene programs","fibrotic monocyte state"],"server":"biorxiv","posted_date":"2026-08-26","authors_short":"Elrod JK, Sanyal A, Hutchins T et al.","categories":[],"topics":["OXPHOS","metabolism","immunology","therapeutics"],"importance_score":79,"url":"https://www.biorxiv.org/content/10.64898/2026.08.21.738279","free_html_url":"https://mito.news/articles/10-64898-2026-08-21-738279","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-21-738279","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744963","doi":"10.64898/2026.08.14.744963","title":"Mitochondrial stress signaling shapes the nuclear response to loss of the chromatin reader MRG-1","headline":"Mitochondrial stress signaling, not just chromatin logic, detaches heterochromatin after MRG-1 loss","blurb":"In C. elegans, losing the euchromatic reader MRG-1 was thought to detach heterochromatin from the nuclear periphery by an unknown indirect route. That route is in part a mitochondrial stress response. The PMK-3/MAPK…","why_bots_should_care":"A genetic split of a chromatin phenotype into mitochondrial-stress-dependent and -independent pieces. Use it when nuclear-organization screens might actually be scoring metabolic stress.","key_claims":["Loss of MRG-1 activates a mitochondrial stress response in C. elegans.","Genetic ablation of the PMK-3/MAPK mitochondrial-stress regulator CBP-3 contributes to detachment of a heterochromatic reporter from the nuclear periphery.","CBP-3 accounts for approximately one-third of the transcriptional changes induced by mrg-1 depletion."],"confidence":"medium","keywords":["MRG-1","CBP-3","PMK-3","heterochromatin","mitochondrial stress","C. elegans"],"dysfunction_signals":["mitochondrial stress after MRG-1 loss","exacerbated mitochondrial dysfunction without CBP-3","fertility defects and embryonic lethality","stress-dependent heterochromatin detachment"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Zaratiegui C, Rezende Pabst F, Rodriguez Palero M et al.","categories":[],"topics":["mito-nuclear communication","stress signaling","chromatin","development","quality control"],"importance_score":79,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744963","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744963","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744963","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-12-744485","doi":"10.64898/2026.08.12.744485","title":"Mycoplasma gallisepticum uses itaconate-associated mitochondrial inhibition to suppress host immunometabolism","headline":"Mycoplasma gallisepticum raises itaconate in finch PBMCs and blocks the SDH-linked immune burst","blurb":"In house finches, live Mycoplasma gallisepticum (MG) suppresses the early circulating immune-metabolic burst that heat-killed MG elicits. Heat-killed bacteria raise succinate dehydrogenase (SDH)-dependent respiration in…","why_bots_should_care":"An in vivo wild-songbird infection with paired PBMC respirometry, itaconate quantification, and a pharmacologic itaconate phenocopy. Use as a pathogen-immunometabolism and SDH-suppression reference.","key_claims":["Heat-killed MG increases SDH-dependent mitochondrial respiration in PBMCs and cytokine gene expression in erythrocytes; live MG does not, and instead increases itaconate in PBMCs.","Dimethyl itaconate administration reproduces the suppressed metabolic and immune phenotype in blood cells seen with live MG.","In eyelid conjunctiva, live MG increases mitochondrial respiration and cytokine gene expression; other treatments do not."],"confidence":"medium","keywords":["Mycoplasma gallisepticum","itaconate","SDH","house finch","PBMC","immunometabolism"],"dysfunction_signals":["itaconate-associated SDH-linked respiratory suppression","failed circulating cytokine induction to live MG","compartmental mitochondrial activation at conjunctiva"],"server":"biorxiv","posted_date":"2026-08-14","authors_short":"Coulson SZ, Eric R, Ramanathan C et al.","categories":[],"topics":["immunology","OXPHOS","metabolism","infection","immunometabolism"],"importance_score":79,"url":"https://www.biorxiv.org/content/10.64898/2026.08.12.744485","free_html_url":"https://mito.news/articles/10-64898-2026-08-12-744485","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-12-744485","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-09-743791","doi":"10.64898/2026.08.09.743791","title":"Mitochondrial Signaling: Nitric Oxide Synthesis by Cytochrome c Oxidase and Its Oxygen Sensitivity Are Modulated by Adenine Nucleotides","headline":"ADP keeps cytochrome oxidase’s nitrite-to-NO activity alive even in high oxygen, in an isoform-specific way","blurb":"Detergent-solubilized yeast and mouse-brain cytochrome c oxidase (Cco) can reduce 1 mM nitrite to nitric oxide when driven by ascorbate/TMPD/cytochrome c. ADP and ATP gate that Cco/NO activity differently. ADP extends…","why_bots_should_care":"A quantitative, isoform-aware Cco/NO study that refuses to overclaim physiological contribution. Use as a Complex-IV nitrite-reductase and adenine-nucleotide-gating reference.","key_claims":["Solubilized yeast and mouse-brain Cco reduce 1 mM nitrite to NO with an ascorbate/TMPD/cytochrome c donor system.","ADP and ATP differentially modulate Cco/NO; ADP extends NO formation across the full oxygen range tested (up to 175 µM O2).","Nucleotide regulation is isoform-dependent: ATP slightly inhibits Va-Cco and strongly stimulates Vb-Cco under anoxia."],"confidence":"medium","keywords":["cytochrome c oxidase","nitrite","NO","ADP","ATP","Cco/NO"],"dysfunction_signals":["hypoxia-shifted ADP/ATP and Cco/NO activity","isoform-dependent nucleotide gating of Complex IV nitrite reduction"],"server":"biorxiv","posted_date":"2026-08-10","authors_short":"Castello PR, Ball KA, Poyton RO","categories":[],"topics":["OXPHOS","redox biology","signaling","hypoxia"],"importance_score":79,"url":"https://www.biorxiv.org/content/10.64898/2026.08.09.743791","free_html_url":"https://mito.news/articles/10-64898-2026-08-09-743791","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-09-743791","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-09-01-748704","doi":"10.64898/2026.09.01.748704","title":"Arabidopsis thaliana ACTIN DEPOLYMERIZING FACTORs are novel susceptibility factors for Colletotrichum higginsianum","headline":"Plant ADF proteins keep PEN2-linked mitochondria off fungal entry sites and help Colletotrichum in","blurb":"Subclass I actin depolymerizing factors (ADF1 through ADF4) in Arabidopsis thaliana act as susceptibility factors for the hemibiotrophic fungus Colletotrichum higginsianum. Losing ADF4, or silencing the whole subclass…","why_bots_should_care":"This is a plant immunity paper whose mitochondrial sentence is positional, not bioenergetic. Mitochondria are part of the PEN2 penetration-resistance kit. Host ADF-dependent actin remodeling appears to keep those mitochondria from stacking at the fungal entry site. Index it with…","key_claims":["Among 11 Arabidopsis ADFs, subclass I (ADF1, ADF2, ADF3, ADF4) is expressed throughout the plant.","adf4 knockouts and ADF1-4 RNA-interference plants are more resistant to Colletotrichum higginsianum.","Both fungal penetration and secondary hyphae formation are suppressed in those genotypes."],"confidence":"medium","keywords":["ADF4","actin depolymerizing factor","PEN2","Colletotrichum higginsianum","mitochondria","penetration resistance","Arabidopsis"],"dysfunction_signals":["infection-induced actin-filament fragmentation","failed mitochondrial recruitment to entry sites","host susceptibility via ADF subclass I"],"server":"biorxiv","posted_date":"2026-09-03","authors_short":"Ohashi M, Aoki S, Shimada TL et al.","categories":[],"topics":["immunology","mitochondrial dynamics","genetics"],"importance_score":78,"url":"https://www.biorxiv.org/content/10.64898/2026.09.01.748704","free_html_url":"https://mito.news/articles/10-64898-2026-09-01-748704","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-09-01-748704","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-18-745425","doi":"10.64898/2026.08.18.745425","title":"The dual PPAR-α/δ agonist elafibranor attenuates TGF-β 1 -induced cardiac fibrosis through redox-metabolic and bioenergetic reprogramming in human cardiac models","headline":"Liver-approved PPAR-α/δ agonist elafibranor eases TGF-β1 fibrosis and restores respiration in human cardiac models","blurb":"Elafibranor, a dual peroxisome proliferator-activated receptor alpha/delta (PPAR-α/δ) agonist already approved for liver disease, blunts transforming growth factor beta 1 (TGF-β1) fibrosis programs in human cardiac…","why_bots_should_care":"A licensed metabolic agonist with a mitochondrial respiration readout across four human cardiac models. Use it as a fibroblast-bioenergetics and PPAR cardiac-fibrosis reference, not as a prescribing note.","key_claims":["At non-cytotoxic concentrations, elafibranor attenuates TGF-β1-driven fibrosis responses across 2D primary cardiac fibroblasts, 3D fibroblast spheroids, contracting 3D cardiac microtissues, and hiPSC-derived cardiomyocytes.","In 2D fibroblasts it reduces myofibroblast differentiation and procollagen 1α1 secretion and partially restores mitochondrial respiratory capacity.","In spheroids it preserves viability, attenuates caspase-3/7 activation, and suppresses procollagen 1α1 release."],"confidence":"medium","keywords":["elafibranor","PPAR","TGF-β1","cardiac fibrosis","NAD","hiPSC","microtissue"],"dysfunction_signals":["TGF-β1-driven loss of mitochondrial respiratory capacity","myofibroblast activation and ECM accumulation","altered NAD and adenine-nucleotide pools","impaired microtissue contraction"],"server":"biorxiv","posted_date":"2026-08-19","authors_short":"Paw M, Minder L, Laimbacher A et al.","categories":[],"topics":["therapeutics","cardiology","OXPHOS","metabolism","redox biology","fibrosis"],"importance_score":78,"url":"https://www.biorxiv.org/content/10.64898/2026.08.18.745425","free_html_url":"https://mito.news/articles/10-64898-2026-08-18-745425","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-18-745425","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-13-744642","doi":"10.64898/2026.08.13.744642","title":"Tyrosine phosphorylation and dimerization cooperatively activate NAMPT to enable NAD+ synthesis in cancer","headline":"Oncogenic tyrosine kinases phosphorylate NAMPT at Y188 and turn on NAD+ salvage, including at mitochondria","blurb":"Nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting NAD+ salvage enzyme, is a direct substrate of proto-oncogenic tyrosine kinases (ALK, insulin receptor, IGF1R, PDGFRA). Phosphoproteomics name Y188 as the…","why_bots_should_care":"A kinase-to-NAD+ switch with an explicit mitochondrial localization of the NAMPT–ALK pair and a residue (Y188) you can mutate. Use as an oncogene-metabolism and NAD-salvage reference.","key_claims":["NAMPT is a direct substrate of ALK, insulin receptor, IGF1R, and PDGFRA; Y188 is the major phosphorylation site, including for NPM1::ALK.","NAMPT interacts with NPM1::ALK in cytoplasm, nucleus, and mitochondria; Y188 phosphorylation enhances catalysis, NMN/NAD+ biosynthesis, and downstream metabolism.","Y188F reduces enzymatic activity, proliferation, and clonogenicity; disrupting dimerization similarly impairs phosphorylation and function."],"confidence":"medium","keywords":["NAMPT","Y188","NAD+","ALK","NMN","dimerization"],"dysfunction_signals":["kinase-activated NAD+ salvage","NAMPT–ALK mitochondrial interaction","NAMPT dependence in ALK-resistant lymphoma"],"server":"biorxiv","posted_date":"2026-08-15","authors_short":"Basappa J, Lobello C, Faustino AM et al.","categories":[],"topics":["metabolism","cancer","NAD","signaling","therapeutics"],"importance_score":78,"url":"https://www.biorxiv.org/content/10.64898/2026.08.13.744642","free_html_url":"https://mito.news/articles/10-64898-2026-08-13-744642","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-13-744642","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-11-26358095","doi":"10.64898/2026.08.11.26358095","title":"Dominant truncating variants in KAT6A cause two neurodevelopmental disorders with opposite gene regulatory and metabolic changes.","headline":"Early KAT6A truncations empty the gene; late ones invert neuronal metabolism and mitochondria","blurb":"Arboleda-Tham syndrome is not one molecular disease. In patient iPSCs, early-truncating KAT6A variants (exons 1–15) are loss-of-function via nonsense-mediated decay; late-truncating variants (exons 16–17) escape NMD and…","why_bots_should_care":"A variant-position split that inverts mitochondrial physiology in patient iPSCs and implies opposite drugs. Use as a Mendelian-precision and mito-epigenetics reference, not as a completed trial.","key_claims":["Early-truncating KAT6A variants (exons 1–15) cause loss-of-function via NMD; late-truncating variants (exons 16–17) escape NMD and cause gain-of-function.","The two classes have distinctive facial gestalt and DNA-methylation episignatures.","They invert the direction of change across neuronal gene regulation, metabolism, and mitochondrial physiology in patient-derived iPSCs with multi-omics."],"confidence":"medium","keywords":["KAT6A","ARTHS","NMD","iPSC","episignature"],"dysfunction_signals":["inverted mitochondrial physiology by KAT6A variant class","opposite metabolic programs in patient iPSCs"],"server":"medrxiv","posted_date":"2026-08-14","authors_short":"Nava AA, Perez-Rodriguez Y, Hsieh T et al.","categories":[],"topics":["neurobiology","metabolism","epigenetics","mtDNA","rare disease"],"importance_score":78,"url":"https://www.medrxiv.org/content/10.64898/2026.08.11.26358095","free_html_url":"https://mito.news/articles/10-64898-2026-08-11-26358095","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-11-26358095","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-07-743627","doi":"10.64898/2026.08.07.743627","title":"Distinct mitochondrial phenotypes align with visual and semantic representations across human cortex","headline":"Visual cortex sits on mitochondria-poor tissue; semantic cortex sits on mitochondria-rich tissue","blurb":"7T fMRI during natural-scene viewing, split by image-to-brain encoding into variance unique to visual versus semantic features, was compared with postmortem mitochondrial atlases under spatial-autocorrelation-preserving…","why_bots_should_care":"A human-cortex result that opposite information axes have opposite mitochondrial anatomies. Use as a cognitive-bioenergetics brief. It is alignment, not causation.","key_claims":["Unique visual versus semantic cortical variance was isolated with 7T fMRI, encoding models, and spatial-autocorrelation-preserving inference.","Visual-specific variance aligns negatively with mitochondrial density and respiratory capacity.","Semantic-specific variance aligns positively with mitochondrial density."],"confidence":"medium","keywords":["7T fMRI","semantic","visual","mitochondrial density","cortex"],"dysfunction_signals":[],"server":"biorxiv","posted_date":"2026-08-08","authors_short":"Lu Z, Wang Y","categories":[],"topics":["neurobiology","OXPHOS","metabolism","computational"],"importance_score":78,"url":"https://www.biorxiv.org/content/10.64898/2026.08.07.743627","free_html_url":"https://mito.news/articles/10-64898-2026-08-07-743627","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-07-743627","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-20-746082","doi":"10.64898/2026.08.20.746082","title":"A Standardized In Vitro Platform for Senolytic Drug Discovery in Human Musculoskeletal Cells","headline":"TLR2 plus peroxide senescence in human disc cells opens a metabolic-activity window for senolytic screens","blurb":"Cherif and colleagues build a standardized senescence recipe for primary human intervertebral disc cells — TLR2 ligand plus tert-butyl hydroperoxide — and show that Alamar Blue can find a senolytic therapeutic window…","why_bots_should_care":"This is a methods paper with a mitochondrial stressor (tBHP-driven ROS) and a bioenergetic readout (metabolic activity) as the screen. Agents building senolytic pipelines for musculoskeletal tissue should ingest the induction pair, the oAF-as-strongest-responder note, and the…","key_claims":["Combined Pam2CSK4 (TLR2 activation) and tBHP (ROS generator) induced a robust senescent phenotype in primary human nucleus pulposus, inner annulus fibrosus, and outer annulus fibrosus cells.","Outer AF cells showed the strongest increases in β-galactosidase fluorescence, β-gal enzymatic activity, and p16.","Alamar Blue distinguished senolytic activity in mixed senescent/non-senescent oAF populations from cytotoxicity in non-senescent cells."],"confidence":"medium","keywords":["senolytic","intervertebral disc","tBHP","TLR2","Alamar Blue","p16","o-Vanillin","ABT-199"],"dysfunction_signals":["oxidative_stress","tlr2_inflammation","senescence","metabolic_activity_drop"],"server":"biorxiv","posted_date":"2026-08-21","authors_short":"Cherif H, Alsabri S, Ouellet JA et al.","categories":[],"topics":["aging","therapeutics","redox biology","metabolism"],"importance_score":77,"url":"https://www.biorxiv.org/content/10.64898/2026.08.20.746082","free_html_url":"https://mito.news/articles/10-64898-2026-08-20-746082","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-20-746082","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-14-744823","doi":"10.64898/2026.08.14.744823","title":"Z-AAT impairs organelle homeostasis and reduces adaptive response to lipids in alpha-1 antitrypsin deficiency models","headline":"Z-AAT polymers clog hepatic lipid handling and leave mitochondria numerous but respiratory-poor","blurb":"Z-variant alpha-1 antitrypsin (Z-AAT) polymers accumulate in Z-HepG2 cells and patient-derived ZZ hepatic organoids, cut secretion, and bring lipid storage, mitochondrial structural abnormalities, more mitochondria with…","why_bots_should_care":"Patient organoids plus a cell line, with mitochondria and peroxisomes scored together under a classic proteotoxic allele. Use as an AATD immunometabolism and lipid-flexibility reference, not as a drug screen.","key_claims":["Z-AAT expression causes intracellular polymer accumulation and reduced secretion in Z-HepG2 cells and ZZ patient hepatic organoids.","Cells accumulate lipid, show mitochondrial structural abnormalities, and increase mitochondrial number while impairing respiratory capacity.","Metabolic profiling shows reduced oxidative phosphorylation and partial reliance on glucose; peroxisomal mass increases."],"confidence":"medium","keywords":["AATD","Z-AAT","HepG2","organoid","peroxisome","lipid","OXPHOS"],"dysfunction_signals":["impaired mitochondrial respiratory capacity","mitochondrial structural abnormalities","blunted lipid-adaptive mitochondrial transcription","increased peroxisomal mass and lipid accumulation"],"server":"biorxiv","posted_date":"2026-08-15","authors_short":"Gil-Martín S, Matamala N, Hagen-Doval O et al.","categories":[],"topics":["metabolism","OXPHOS","proteostasis","liver","organelle homeostasis"],"importance_score":77,"url":"https://www.biorxiv.org/content/10.64898/2026.08.14.744823","free_html_url":"https://mito.news/articles/10-64898-2026-08-14-744823","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-14-744823","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-08-743687","doi":"10.64898/2026.08.08.743687","title":"MAFB is essential for the maintenance of adult human α-cell identity and glucagon secretion","headline":"MAFB is essential for the maintenance of adult human α-cell identity and glucagon secretion","blurb":"Scientific focus: OXPHOS, redox biology, computational. Core claim (from abstract): Using shRNA-mediated MAFB knockdown (KD) in whole and CD26+ α-cell-enriched human pseudoislets, we found that whole pseudoislet MAFB KD…","why_bots_should_care":"For mitochondrial biologists focused on OXPHOS, redox biology, computational, this preprint is worth full-text review soon. Abstract-level takeaway: Using shRNA-mediated MAFB knockdown (KD) in whole and CD26+ α-cell-enriched human pseudoislets, we found that whole pseudoislet…","key_claims":["Using shRNA-mediated MAFB knockdown (KD) in whole and CD26+ α-cell-enriched human pseudoislets, we found that whole pseudoislet MAFB KD impaired glucagon synthesis and secretion while only modestly reducing insulin content and cAMP-potentiated insulin release.","In addition, MAFB-dependent downregulation of electron transport chain genes was confined to a large α-cell subcluster, manifesting as impaired islet-wide mitochondrial respiration within the broader α-cell population.","Together, these findings identify MAFB as an essential adult human α-cell maintenance factor that links diabetes-associated downregulation to impaired glucagon secretion, α-cell identity erosion, and mitochondrial dysfunction."],"confidence":"medium","keywords":["mitochondria","OXPHOS","redox biology","computational","mitochondrial dysfunction","functional impairment","OXPHOS / ETC","systemic metabolic stress"],"dysfunction_signals":["mitochondrial dysfunction","functional impairment","OXPHOS / ETC","systemic metabolic stress"],"server":"biorxiv","posted_date":"2026-08-14","authors_short":"Coate K, Liu J, Guo M et al.","categories":[],"topics":["OXPHOS","redox biology","computational"],"importance_score":77,"url":"https://www.biorxiv.org/content/10.64898/2026.08.08.743687","free_html_url":"https://mito.news/articles/10-64898-2026-08-08-743687","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-08-743687","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-17-745291","doi":"10.64898/2026.08.17.745291","title":"Low-heteroplasmy mitochondrial DNA mutations improve clonal reconstruction of human cells","headline":"Low-heteroplasmy mitochondrial DNA mutations improve clonal reconstruction of human cells","blurb":"Scientific focus: mtDNA, aging. Core claim (from abstract): Somatic mitochondrial DNA (mtDNA) mutations act as endogenous single-cell barcodes measurable alongside cell-state profiles, but lineage tracing has…","why_bots_should_care":"For mitochondrial biologists focused on mtDNA, aging, this preprint is worth full-text review soon. Abstract-level takeaway: Somatic mitochondrial DNA (mtDNA) mutations act as endogenous single-cell barcodes measurable alongside cell-state profiles, but lineage tracing has…","key_claims":["Somatic mitochondrial DNA (mtDNA) mutations act as endogenous single-cell barcodes measurable alongside cell-state profiles, but lineage tracing has traditionally focused on high-heteroplasmy variants, which are easier to detect but few and potentially shaped by selection.","Using lentiviral barcoding of human hematopoietic cells to establish ground-truth clone identities, we show that after stringent molecule-level error filtering, mutation calls below 10% per-cell heteroplasmy account for roughly half of all lineage-informative calls.","Retaining the full heteroplasmy spectrum approximately doubled the clonal-assignment area under the precision-recall curve relative to a >10% cutoff, and single-molecule-supported calls improved recovery when retained collectively."],"confidence":"medium","keywords":["mitochondria","mtDNA","aging","disease context"],"dysfunction_signals":["mtDNA","disease context","aging"],"server":"biorxiv","posted_date":"2026-08-21","authors_short":"weng c, Gao T, Colgan W et al.","categories":[],"topics":["mtDNA","aging"],"importance_score":76,"url":"https://www.biorxiv.org/content/10.64898/2026.08.17.745291","free_html_url":"https://mito.news/articles/10-64898-2026-08-17-745291","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-17-745291","free_note":"Teaser only (title + blurb + ranking fields). Free full HTML at free_html_url. Bots: pay x402 at paid_endpoint for mitos.brief.v1 JSON. No body_markdown here."},{"id":"10-64898-2026-08-19-745850","doi":"10.64898/2026.08.19.745850","title":"Upregulation of the Unfolded and Mitochondrial Unfolded Protein Responses in Oxidative Stress-Induced Cataract","headline":"Peroxide cataracts in zebrafish switch on the unfolded and mitochondrial unfolded protein responses","blurb":"Hydrogen peroxide injected into the aqueous humor of adult zebrafish produces cortical cataracts and a cortex proteome that activates the unfolded and mitochondrial unfolded protein responses, alongside…","why_bots_should_care":"An in vivo oxidative-cataract model with DIA-PASEF cortex proteomics that names mitoUPR explicitly. Use it as a lens proteostasis-and-organelle-stress reference, not as a human treatment map.","key_claims":["Hydrogen peroxide injected into zebrafish aqueous humor induces cortical cataracts.","nrf2fh318/fh318 models reduced oxidative-stress protection of aged human lenses; cryaba-/- models impaired lens proteostasis; a double mutant combines both.","DIA-PASEF proteomics of the cortex shows genotype- and day-dependent activation of the unfolded and mitochondrial unfolded protein responses."],"confidence":"medium","keywords":["cataract","mitoUPR","UPR","NRF2","cryaba","zebrafish","DIA-PASEF","oxidative stress"],"dysfunction_signals":["oxidative cortical cataract","UPR and mitoUPR activation","energy-metabolism and calcium remodeling","impaired NRF2 defense and crystallin proteostasis"],"server":"biorxiv","posted_date":"2026-08-20","authors_short":"Zelle SR, McDonald WH, Mchaourab HS et al.","categories":[],"topics":["proteostasis","redox biology","metabolism","ophthalmology","mitoUPR"],"importance_score":76,"url":"https://www.biorxiv.org/content/10.64898/2026.08.19.745850","free_html_url":"https://mito.news/articles/10-64898-2026-08-19-745850","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-08-19-745850","free_note":"Teaser only (title + blurb + ranking fields). 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