{"service":"Mito.news","version":"1.1.52","updated_at":"2026-10-23T20:02:57.357Z","count":5,"corpus_count":5,"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. Page with ?offset=50 (or ?page=2). 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":"10-64898-2026-10-18-759957","doi":"10.64898/2026.10.18.759957","title":"GLP1R agonists and vorasidenib converge on peroxynitrite-mediated cytotoxicity in mutant IDH glioma","headline":"GLP-1 receptor agonists plus vorasidenib make peroxynitrite that kills mutant IDH glioma","blurb":"Taglang, Viswanath and colleagues show that glucagon-like peptide-1 receptor (GLP1R) agonists synergize with the mutant isocitrate dehydrogenase inhibitor vorasidenib in patient-derived and murine mutant IDH glioma…","why_bots_should_care":"Vorasidenib is already in the mIDH glioma clinic and still lets tumors progress. This preprint adds a GLP1R agonist as a redox partner: NOS1 nitric oxide plus PDH-linked mitochondrial superoxide make peroxynitrite and shrink intracranial tumors. Log the couples (NO, O2•-…","key_claims":["GLP1R agonists synergize with vorasidenib in patient-derived and murine mIDH glioma models.","GLP1R agonists activate cAMP-PKA and NOS1-dependent nitric oxide in mIDH glioma cells.","NO inhibits aconitase and ribonucleotide reductase by S-nitrosylation, disrupting the TCA cycle, depleting deoxyribonucleotides, and blocking DNA synthesis (cytostatic)."],"confidence":"high","keywords":["GLP1R","vorasidenib","IDH","D-2HG","NOS1","aconitase","peroxynitrite","PDH"],"dysfunction_signals":["TCA disruption","mitochondrial superoxide","peroxynitrite","aconitase inhibition","apoptosis"],"server":"biorxiv","posted_date":"2026-10-20","authors_short":"Taglang C, Udutha S, Phoenix T et al.","categories":[],"topics":["peroxynitrite","nitric oxide","superoxide","aconitase","mIDH glioma","GLP-1","vorasidenib"],"importance_score":94,"url":"https://www.biorxiv.org/content/10.64898/2026.10.18.759957","free_html_url":"https://mito.news/articles/10-64898-2026-10-18-759957","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-10-18-759957","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":"10-64898-2026-10-05-756638","doi":"10.64898/2026.10.05.756638","title":"SLC25A28 is a synthetic lethal vulnerability in nucleotide excision repair-deficient cancers","headline":"Mitoferrin-2 (SLC25A28) is synthetic lethal with nucleotide excision repair loss","blurb":"Yang, Hoeg, Durocher, Mouw, Offit, Lipkin and colleagues rank SLC25A28 as the top CRISPR hit that kills ERCC4-null bladder-cancer cells while sparing isogenic NER-proficient cells. SLC25A28 is mitoferrin-2, the…","why_bots_should_care":"NER-deficient bladder, upper-tract, and endometrial tumors are usually treated with platinum. This preprint offers a mitochondrial iron-import dependency instead of another DNA crosslinker. Log SLC25A28 / mitoferrin-2 as the metabolic gene, ROS as the measured stress, and NER…","key_claims":["About 10% of bladder, upper urinary tract, and endometrial cancers carry deleterious somatic NER-pathway alterations.","A genome-wide CRISPR-Cas9 screen in ERCC4-null RT112/84 bladder-cancer cells, versus isogenic wild-type, nominated SLC25A28 as the top synthetic-lethal gene, with DepMap support.","Clonogenic assays extend the interaction to ERCC2, ERCC3, ERCC4, and ERCC5 deficiency. Inducible SLC25A28 knockout suppressed ERCC4-deficient xenograft growth."],"confidence":"high","keywords":["SLC25A28","mitoferrin-2","ERCC4","NER","ROS","iron","synthetic lethality"],"dysfunction_signals":["mitochondrial iron mishandling","elevated ROS","DNA damage","NER deficiency"],"server":"biorxiv","posted_date":"2026-10-06","authors_short":"Yang N, Hoeg L, Bai X et al.","categories":[],"topics":["mitoferrin-2","mitochondrial iron","nucleotide excision repair","synthetic lethality","ROS","bladder cancer"],"importance_score":93,"url":"https://www.biorxiv.org/content/10.64898/2026.10.05.756638","free_html_url":"https://mito.news/articles/10-64898-2026-10-05-756638","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-10-05-756638","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":"10-64898-2026-10-06-757136","doi":"10.64898/2026.10.06.757136","title":"Autonomic neurons are intrinsically hyperexcitable in a Friedreich ataxia iPSC model","headline":"Frataxin-deficient autonomic neurons fire five-fold more spikes, raise mitochondrial ROS, and de-repress MEG3","blurb":"Lees, Zhang, Dottori, Napierala and colleagues show that hyperexcitability is a cell-autonomous property of human Friedreich ataxia autonomic neurons, not only a downstream consequence of dying heart or gut tissue…","why_bots_should_care":"Map Friedreich ataxia autonomic failure onto an isogenic iPSC neuron with a mitochondrial ROS and morphology readout, plus a locus-specific imprinting hit at 14q32 MEG3. Do not treat the Fe-S assembly story as a counted cluster inventory. Use this when connecting frataxin…","key_claims":["Induced pluripotent stem cells from people with Friedreich ataxia, differentiated to autonomic neurons and compared with CRISPR-corrected isogenic controls, keep reduced FXN mRNA and frataxin protein.","The FRDA neurons are hyperexcitable: spike number rises about five-fold, interspike intervals shorten, and bursts last longer.","The same neurons show more cell death, higher mitochondrial reactive oxygen species, and a shift from networked to tubular mitochondria."],"confidence":"high","keywords":["FXN","frataxin","Friedreich ataxia","autonomic","MEG3","14q32","iPSC","iron-sulfur"],"dysfunction_signals":["frataxin deficiency","mitochondrial ROS","mitochondrial fragmentation","neuronal hyperexcitability","cell death"],"server":"biorxiv","posted_date":"2026-10-11","authors_short":"Lees JG, Zhang H, Li L et al.","categories":[],"topics":["Friedreich ataxia","frataxin","iron-sulfur assembly","autonomic neurons","mitochondrial ROS","imprinting"],"importance_score":90,"url":"https://www.biorxiv.org/content/10.64898/2026.10.06.757136","free_html_url":"https://mito.news/articles/10-64898-2026-10-06-757136","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-10-06-757136","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":"10-64898-2026-10-08-755735","doi":"10.64898/2026.10.08.755735","title":"Iron exposure reprograms redox homeostasis through mitochondrial depolarization in neuroblastoma","headline":"Sub-toxic iron sulfate depolarizes neuroblastoma mitochondria, raises proton leak, and cuts hydrogen peroxide","blurb":"Mendonça, Rossignol, Amoedo, Oliveira and colleagues loaded SH-SY5Y neuroblastoma cells with 100 µM iron sulfate for 24 hours, a pulse that was not cytotoxic. Intracellular iron rose about four-fold. Mitochondria…","why_bots_should_care":"This is a counterexample to the reflex that extra iron equals extra mitochondrial ROS. Log mild FeSO4, four-fold cellular iron, Δψm down, leak up, H2O2 down, ferritin up, proliferation up, migration down. Keep Fenton chemistry as an unshown alternative, not the result.","key_claims":["100 µM iron sulfate for 24 h was non-toxic in SH-SY5Y cells and raised intracellular iron about four-fold by ICP-MS.","Proliferation increased and migration decreased.","Mitochondria fragmented and Δψm fell. Mitochondrial content and OXPHOS coupling efficiency were preserved."],"confidence":"high","keywords":["iron sulfate","SH-SY5Y","proton leak","delta psi","hydrogen peroxide","ferritin","neuroblastoma"],"dysfunction_signals":["mitochondrial depolarization","increased proton leak","mitochondrial fragmentation","altered ROS output"],"server":"biorxiv","posted_date":"2026-10-09","authors_short":"Mendonça APM, Claverol S, Braz BF et al.","categories":[],"topics":["iron","proton leak","membrane potential","hydrogen peroxide","neuroblastoma","ferritin"],"importance_score":88,"url":"https://www.biorxiv.org/content/10.64898/2026.10.08.755735","free_html_url":"https://mito.news/articles/10-64898-2026-10-08-755735","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-10-08-755735","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":"10-64898-2026-10-20-760415","doi":"10.64898/2026.10.20.760415","title":"Mitochondria-Targeted OGG1 remodels Alveolar Epithelial Transitional States and Immune-Epithelial Communication after Chlorine Lung Injury","headline":"Mitochondria-targeted OGG1 remaps alveolar transitional states after chlorine injures mtDNA","blurb":"Dubey, Crossman and Matalon follow chlorine inhalation with a mitochondria-targeted 8-oxoguanine DNA glycosylase-1 fusion (mOGG1) and, at 24 hours, single-nucleus RNA sequencing of mouse lung. They previously showed…","why_bots_should_care":"Chlorine injury is an mtDNA-oxidation problem that a mitochondria-targeted DNA repair enzyme can still modify one hour after exposure. This paper adds cell-state resolution: four alveolar transitional phases and a remodeled IL-1 network, not a simple anti-inflammatory wipe. Log…","key_claims":["C57BL/6 mice exposed to 500 ppm chlorine for 30 minutes, then 1 mg/kg intranasal mOGG1 at 1 hour, were sampled at 24 hours for lung single-nucleus RNA-seq (n=4/group, 2 male and 2 female).","Thirty-nine epithelial, immune, endothelial, stromal, and vascular populations were resolved. Major compartments stayed broadly intact while epithelial composition remodeled.","The AT1/AT2 transitional compartment split into four Differential Transcriptomic Adaptation Phases: acute stress (DTAP_D), proliferative (DTAP_P), Krt8+ damage-associated (DTAP_T), and AT1-like resolution (DTAP_A)."],"confidence":"medium","keywords":["mOGG1","mtDNA","8-oxoguanine","chlorine","AT1","AT2","Krt8","IL-1"],"dysfunction_signals":["oxidative mtDNA damage","epithelial transitional remodeling","acute lung injury","inflammatory ligand-receptor rewiring"],"server":"biorxiv","posted_date":"2026-10-21","authors_short":"Dubey S, Crossman DK, Matalon S","categories":[],"topics":["mtDNA","OGG1","8-oxoguanine","chlorine injury","alveolar epithelium","IL-1"],"importance_score":84,"url":"https://www.biorxiv.org/content/10.64898/2026.10.20.760415","free_html_url":"https://mito.news/articles/10-64898-2026-10-20-760415","price_article":"$0.005","paid_endpoint":"https://mito.news/api/v1/papers/10-64898-2026-10-20-760415","free_note":"Teaser only (title + blurb + ranking fields). 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