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Mitochondria importance articles
Abstract-level scientific briefs on mitochondria preprints—structured for researchers and agents. Free in the browser. Machine JSON remains available via x402 for bots.
34 of 176 articles · updated 2026-09-18T14:04Z
- biorxiv2026-08-12score 91OXPHOSmetabolismredox biology
Clever-1 sits on AML mitochondria, feeds complex IV with lipoprotein lipid, and is a bexmarilimab-sensitive OXPHOS liability
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 capacity. Antibody blockade (bexmarilimab) collapses that program, hardest in OXPHOS-high models and under lipid restriction.
Source preprint: Clever-1 blockade disrupts lipid metabolism and mitochondrial fitness in acute myeloid leukemia
- biorxiv2026-09-07score 89cancerOXPHOSfusion
Triple-negative cells that survive radiation rebuild mitochondria through the short OPA1 isoform
After ionizing radiation, residual triple-negative breast-cancer cells swell their mitochondrial mass, cristae, oxidative phosphorylation, and metabolites, then largely revert when they regrow. The short OPA1 isoform rises in the residual state; OPA1 knockout erases the rewiring, and genetic or drug OPA1 blockade improves the radiation response.
Source preprint: Mitochondrial rewiring supports survival of triple negative breast cancer cells after ionizing radiation
- biorxiv2026-08-20score 89cancerOXPHOSredox biology
HES1-low senescent CTCs keep OXPHOS and SOD1 — and those are the cells that regrow metastases
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 cells. HES1 binds the Sod1 promoter and represses it; dual SOD1 inhibition plus ABT737 hits both residual pools in vivo.
Source preprint: The HES1-SOD1 Antagonism Shapes Senescence Heterogeneity and Impacts Metastatic Relapse of Circulating Tumor Cells
- biorxiv2026-08-19score 88mitochondrial dynamicsmitophagyredox biology
MICOS Chchd3 loss breaks the fly heart through mitophagy, ROS, and ER stress — not ROS alone
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 contractility; Xbp1 does the same for ER stress. Catalase knockdown raises ROS without hurting the heart. Congenital-heart-disease candidate MICOS failure is a multi-stress organelle problem, not a single oxidant dump.
Source preprint: Deficiency in MICOS component Chchd3 Compromises Drosophila Heart Function via mitophagy, ROS and ER Stress
- biorxiv2026-08-15score 88OXPHOSredox biologyapoptosis
IVF and vitrification depolarize the blastocyst mitochondrion; the adult mouse heart still shows the bioenergetic scar
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 OXPHOS capacity, more H2O2 per oxygen, altered OXPHOS subunit abundance, and reduced complex I, III and IV activity. The organelle is a plausible lasting carrier of ART cardiovascular risk.
Source preprint: In vitro fertilisation and vitrification disrupt embryo mitochondrial function and redox balance that persists into adulthood in mice
- biorxiv2026-08-11score 87cancertherapeuticsOXPHOS
ClpP agonist TR-107 collapses ACC respiration at nanomolar doses and synergizes with IGF-1R blockade
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 falls, ROS rise, ferroptosis-rheostat proteins come up, and the compound is not an ABCB1 substrate. Combined with IGF-1R inhibitors, the kill is synergistic.
Source preprint: TR-107, a novel mitochondrial ClpP agonist, induces robust antitumor activity against preclinical models of adrenocortical carcinoma
- biorxiv2026-09-09score 86OXPHOSredox biologyiron
Rotenone Complex I block raises mitochondrial iron through ROS, then iron feeds the ROS back
In differentiated dopaminergic neurons, rotenone inhibition of mitochondrial Complex I is enough to mis-place iron: mitochondria and the whole cell gain iron while the cytosol loses labile iron. Reactive oxygen species (ROS) sit in the middle of that shift, and iron then amplifies the same ROS, a loop with a direct line to Parkinson disease and other iron-loading mitochondrial disorders.
Source preprint: Reactive Oxygen Species Generation Drives Iron Accumulation by Rotenone-Mediated Inhibition of Mitochondrial Complex I in Dopaminergic Neurons
- biorxiv2026-09-03score 86mitochondrial dynamicsredox biologymetabolism
Losing ELM1B freezes moss mitochondrial fission, oxidizes the matrix, and weakens stress tolerance
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 propose as a protein-damage mark. Genetic loss of PpELM1B (ELONGATED MITOCHONDRIA 1B) locks that elongated state, shifts matrix glutathione more oxidized, increases EOS red, slows growth and respiration, and makes plants more sensitive to oxidative stress, even though matrix mixing still occurs at the same slow, days-long rate as in wild type.
Source preprint: Loss of ELM1B impairs mitochondrial fission, matrix redox state and stress tolerance in Physcomitrium patens
- biorxiv2026-08-20score 86immunologymitochondrial dynamicstherapeutics
Gelsolin keeps macrophage mitochondria intact during Legionella infection and buys survival without changing bacterial load
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 neutrophils make fewer NETs and lose mitochondrial capacity, and infected macrophages lose mitochondrial network morphology and respiration. Recombinant gelsolin extends survival, reduces lung pathology, and calms the macrophage inflammatory signature. Host mitochondrial integrity, not CFU, is the survival variable.
Source preprint: Gelsolin protects mitochondria and regulates inflammation during Legionella pneumophila infection
- biorxiv2026-08-17score 86OXPHOSredox biologymetabolism
APX2014 rewires mitochondrial cysteine, phospho, and acetyl marks in minutes — the proteome has not moved yet
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 processes are mitochondrial translation, electron transport, TCA metabolism, and mitochondrial redox homeostasis, matching a functional drop in TCA-substrate use.
Source preprint: Integrated Post-Translational Modification (PTM) Proteomics Reveals Early Redox and Mitochondrial Remodeling Following Ref-1 Inhibition in Pancreatic Cancer
- biorxiv2026-09-09score 85redox biologyneurobiologymetabolism
Female hypothalamic microglia resist early obesity with a redox-and-mitochondria program until mTORC1 breaks it
In females, not males, hypothalamic microglia answer a high-fat diet with more antioxidant capacity and a remodeled mitochondrial network, which delays early weight gain. Microglial mTORC1 later wrecks those mitochondria and ends the grace period. Sex-specific obesity risk has an organelle switch in a brain-resident immune cell.
Source preprint: A Female-Specific Microglial Redox Program Gates Susceptibility to Obesity
- biorxiv2026-08-17score 85metabolismtherapeuticscancer
Sertraline plus carfilzomib starves SSP-active T-cell tumors of cholesterol flux and mitochondrial respiration
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 synergistic because they pull cholesterol in opposite directions and together collapse mitochondrial respiration. The pair works in an aggressive MYCN PTCL mouse model and remakes the immune microenvironment, while largely sparing SSP-inactive tumor cells and healthy blood cells.
Source preprint: Sertraline and Carfilzomib Synergize to Target T-cell Malignancies with Serine/Glycine synthesis activity via Cholesterol Dysregulation, Cellular Stress and Immune Modulation
- medrxiv2026-08-11score 84mitochondrial dynamicsmitophagycalcium signaling
De novo MFN2 N311S distorts the GTPase fold, weakens Parkin binding, and fragments cardiomyoblast mitochondria
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 H9c2 lines the mutant protein is scarce, mitochondria cluster and fragment, ΔΨm/ATP/OCR fall, cytosolic Ca2+ and ROS rise, and hypertrophic PI3K/AKT/mTOR plus Myh6/Nppa/Nfatc programs turn on.
Source preprint: A loss-of-function mutation in the GTPase domain of MFN2 , perverting mitochondrial dynamics, is associated with dilated cardiomyopathy
- biorxiv2026-08-19score 83apoptosisredox biologyimmunology
Isoflurane depolarizes CD4 T-cell mitochondria and opens a reversible ROS–p38–caspase death path; propofol does not
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 apoptosis through p38 MAPK. Caspase inhibition, N-acetyl cysteine, and a p38 inhibitor all rescue. Propofol preserves mitochondrial integrity, lowers oxidative stress, and supports higher proliferation. The injury is transient: patients recover postoperatively, and Jurkat cells recover within 24–48 hours of washout.
Source preprint: Differential Impact of Isoflurane and Propofol on Apoptotic Regulation of Helper T cells
- biorxiv2026-08-13score 82metabolismcardiologylipid
2-Hydroxyglutarate parks fatty acids in triglycerides and away from mitochondria and lipotoxic membranes
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 is more potent despite lower accumulation: it raises DGAT-dependent TG synthesis, slows TG turnover, and constrains the ethanolamine Kennedy branch, depleting phosphatidylethanolamine. FAO, long-chain acylcarnitines, and lipid peroxidation fall, independent of pseudohypoxic transcription. In mice L2HG causes hypertriglyceridemia, remakes cardiac TG acyl chains, and limits ischemia-induced cardiac acylcarnitine buildup, matching a human 2HG–triglyceride association. 2HG decides how fat is allocated, not only whether it is burned.
Source preprint: 2-Hydroxyglutarate Redirects Fatty Acid Partitioning to Mitigate Lipotoxic Stress and Preserve Metabolic Fuel
- biorxiv2026-08-17score 81metabolismredox biologyTCA cycle
Chlamydomonas NADK2 parks in mitochondria in the dark; without it the TCA cycle and heterotrophy fail
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 TCA cycle stalls and heterotrophic growth collapses. In the light, chloroplast NADK1 covers energy needs and acetate is rerouted through the glyoxylate shunt, bypassing TCA and cutting mitochondrial ROS. NAD kinase localization is plastic, and bypass metabolism is how the mutant survives daylight.
Source preprint: Dual-targeted NADK2 Links Mitochondrial Redox Homeostasis to Carbon Partitioning and Heterotrophic Growth in Chlamydomonas reinhardtii
- biorxiv2026-09-16score 80infectionmalariabioenergetics
Nutrient stress pushes Plasmodium falciparum into a pre-existing latent state that keeps mitochondria on
Artemisinin kills most Plasmodium falciparum malaria parasites and leaves a few that later recrudesce. Mild nutrient deprivation raises entry into a latent early-trophozoite state two- to three-fold after dihydroartemisinin, and that frequency tracks long-term recovery. The same transcriptional signature is already present, rare, in untreated cultures. Latent parasites throttle growth programs but selectively keep mitochondrial functions, redox control, nutrient uptake, lipid metabolism, and invasion kit.
Source preprint: Environmental stress promotes entry into a pre-existing latent state in Plasmodium falciparum
- biorxiv2026-08-17score 80immunologyOXPHOSmetabolism
HIF-1α makes intestinal RORγt+ Tregs mitochondrially sloppy and inflammatory
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) colitis, T-cell-transfer colitis, and azoxymethane/DSS colitis-associated cancer. Protection can travel with the Treg genotype alone. Those Tregs make more IL-10, less IL-17A and IFN-γ, suppress better, carry fewer dysfunctional and mitochondrial-ROS-high mitochondria, favor fusion-associated transcription, and show higher basal and maximal oxygen consumption and reserve capacity.
Source preprint: HIF-1α integrates metabolic and immunoregulatory programs in RORγt⁺ regulatory T cells during intestinal inflammation
- biorxiv2026-08-10score 79OXPHOSredox biologysignaling
ADP keeps cytochrome oxidase’s nitrite-to-NO activity alive even in high oxygen, in an isoform-specific way
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 measurable NO formation across the whole oxygen range tested, up to 175 µM O2. ATP slightly inhibits Va-containing Cco and strongly stimulates Vb-containing Cco under anoxia. Cellular ADP/ATP and subsequently assayed Cco/NO both rise transiently after a hypoxic shift. The paper claims metabolic and isoform gating of catalytic capacity, not the enzyme’s share of cellular NO at physiological nitrite in coupled mitochondria.
Source preprint: Mitochondrial Signaling: Nitric Oxide Synthesis by Cytochrome c Oxidase and Its Oxygen Sensitivity Are Modulated by Adenine Nucleotides
- biorxiv2026-09-03score 78metabolismhepatologyredox biology
Losing ER NADPH enzyme H6PD fills the liver with triglycerides and slows mitochondrial beta-oxidation
Hexose-6-phosphate dehydrogenase makes NADPH inside the ER. Knock it out in mice and the liver piles unsaturated long-chain triglycerides; Nile red agrees; proteomics turn fatty-acid pathways up. An AML12 CRISPR knockout accumulates lipid, cuts mitochondrial beta-oxidation, and the abstract cuts off mid-assay.
Source preprint: Hexose-6-phosphate dehydrogenase deficiency disrupts hepatic fatty acid homeostasis and induces triglyceride accumulation
- biorxiv2026-08-19score 78therapeuticscardiologyOXPHOS
Liver-approved PPAR-α/δ agonist elafibranor eases TGF-β1 fibrosis and restores respiration in human cardiac models
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 fibroblasts, spheroids, and contracting microtissues while partially restoring mitochondrial respiratory capacity, remodeling NAD and adenine-nucleotide pools, and recovering some calcium-handling and contraction parameters. That is a bioenergetic anti-fibrotic signal in human in-vitro systems, not a clinical cardiomyopathy trial.
Source preprint: The dual PPAR-α/δ agonist elafibranor attenuates TGF-β 1 -induced cardiac fibrosis through redox-metabolic and bioenergetic reprogramming in human cardiac models
- biorxiv2026-09-10score 77cell deathcancerredox biology
Melittin kills liver-cancer cells through mitochondrial ROS and gasdermin E, not only by ripping the plasma membrane
The bee-venom peptide melittin, textbook membrane detergent, drives pyroptosis in hepatocellular carcinoma cells via mitochondrial oxidative stress and gasdermin E (GSDME) cleavage. Scavenge mitochondrial reactive oxygen species (mtROS) with Mito-TEMPO and the lytic death retreats. The peptide still punches membranes. It also turns the mitochondrion into the match.
Source preprint: Melittin-induced membrane disruption in hepatocellular carcinoma involves mtROS/GSDME-mediated pyroptosis
- biorxiv2026-08-21score 77agingtherapeuticsredox biology
TLR2 plus peroxide senescence in human disc cells opens a metabolic-activity window for senolytic screens
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. Outer annulus fibrosus cells senesce hardest. o-Vanillin, RG-7112, and ABT-199 drop metabolic activity in mixed senescent cultures without killing non-senescent cells, and those drops track β-galactosidase and p16.
Source preprint: A Standardized In Vitro Platform for Senolytic Drug Discovery in Human Musculoskeletal Cells
- biorxiv2026-08-20score 76proteostasisredox biologymetabolism
Peroxide cataracts in zebrafish switch on the unfolded and mitochondrial unfolded protein responses
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 energy-metabolism, calcium, degradation, and remodeling shifts. Crossing reduced NRF2 defense with a crystallin/proteostasis mutant (cryaba) is meant to mimic aged human lenses. The mitochondrial claim is not that the lens is a new OXPHOS organ, but that mitoUPR joins UPR as a candidate therapeutic axis in oxidative cataract.
Source preprint: Upregulation of the Unfolded and Mitochondrial Unfolded Protein Responses in Oxidative Stress-Induced Cataract
- biorxiv2026-08-17score 75neurobiologymtDNAmetabolism
Fractionated 20 Gy X-rays senesce F11 sensory neurons and raise mtDNA copy number without a ROS or OCR hit
Four daily 5 Gy X-ray fractions (20 Gy total) leave F11 dorsal-root-ganglion neuron-like cells senescent, with higher mitochondrial DNA copy number and a shifted NAD+/NADH pathway, but without a change in oxygen consumption rate or an oxidative-stress signal 24 hours after the last dose. Gene-expression changes land on mechanoreceptor-fiber programs that can be pro-nociceptive. Radiotherapy-linked chronic pain, in this cell line, is not a simple mitochondrial ROS story.
Source preprint: Fractionated ionising radiation affects cellular functions, and gene expression associated to subpopulation of F11 dorsal root ganglia neurons without inducing oxidative stress
- biorxiv2026-09-04score 74aginggliaredox biology
Doxorubicin and high glucose both senesce human microglia, but only high glucose turns NRF2-TFAM on
HMC3 microglia senesce under chronic doxorubicin or high glucose: hypertrophy, SA-beta-gal, less viability, p53-p21, lingering DNA-damage signaling. Metabolic stress also induces p16 and parks p21 at the nuclear rim. Mitochondria move in both cases: doxorubicin turns NRF2-TFAM down; high glucose turns that axis on and raises KEAP1, an antioxidant reply that still fails to restore mitochondrial content.
Source preprint: Genotoxic and metabolic stress drive divergent senescence programs in human microglia
- biorxiv2026-08-13score 74cancerredox biologyhypoxia
Baicalein plus thermal cycling kills hypoxic A549 cells by dropping HIF-1α/SOD2 and collapsing mitochondrial potential
Under cobalt chloride hypoxia, the flavonoid baicalein plus thermal-cycling stimulation (TCS) cuts A549 non-small-cell lung-cancer viability and drives apoptosis while largely sparing IMR-90 lung fibroblasts. The pair suppresses hypoxia-inducible factor 1-alpha (HIF-1α) and mitochondrial superoxide dismutase 2 (SOD2), raises reactive oxygen species, downregulates the sanitizing enzyme MutT homolog 1 (MTH1), drops mitochondrial membrane potential, and increases poly(ADP-ribose) polymerase (PARP) cleavage.
Source preprint: Combined effect of baicalein and thermal-cycling stimulation on suppressing non-small cell lung cancer A549 cells under CoCl 2 -induced hypoxia
- biorxiv2026-08-17score 73neurobiologyredox biologypain
Schwann-cell p75NTR turns NGF into mitochondrial ROS and TRPA1-dependent persistent pain
Nerve growth factor (NGF) pain splits by receptor and cell. Neuronal TrkA carries acute nociception and heat hyperalgesia. Mechanical allodynia and cold hypersensitivity require p75NTR on Schwann cells. There, NGF and proNGF trigger p75NTR-dependent calcium release, TRPA1 activation, mitochondrial reactive oxygen species, and NOX1-dependent oxidative amplification. Blocking ROS or TRPA1, or deleting Trpa1 in Schwann cells, cuts mechanical and cold pain without touching the acute/heat TrkA program. Cleavage-resistant proNGF only evokes the p75NTR half.
Source preprint: Schwann cell p75NTR sustains persistent pain downstream to NGF through ROS-dependent TRPA1 signaling
- biorxiv2026-08-25score 72redox biologymetabolismtherapeutics
Thiol-coated iron oxide nanoparticles chelate copper and put tomato mitochondria back to work
MPA-iron oxide nanoparticles sequentially coated with chitosan, glutathione, and 3-mercaptopropionic acid bind more copper than bare iron oxide, lower intracellular reactive oxygen species, restore mitochondrial membrane potential, and rescue germination plus root and shoot growth in copper-stressed tomato (Solanum lycopersicum) seedlings. The plant mitochondrion is treated as the first organelle copper wrecks, and as a readable endpoint for a dual chelator-antioxidant particle.
Source preprint: Efficient Mitigation of Copper Induced Cellular Dysfunction Using Chitosan Based Iron Oxide Nanoparticles
- biorxiv2026-08-19score 72neurobiologyredox biologyproteostasis
VCP inhibitor ML240 saves photoreceptors, not RPE, and keeps cytochrome c in inner segments
In a human iPSC-RPE plus porcine neuroretina co-culture, the cigarette-smoke oxidant hydroquinone (HQ) stresses both RPE and photoreceptors, drives caspase apoptosis, ER-associated degradation in photoreceptors, thinner outer nuclear layer, and shorter outer segments. The VCP inhibitor ML240 does not stop HQ apoptosis in iPSC-RPE, but it preserves photoreceptor outer-segment length and cone density. Proteomics show lower ERAD markers, higher antioxidant proteins, and preserved cytochrome c enrichment in inner segments, read as improved mitochondrial integrity.
Source preprint: VCP inhibition preserves photoreceptor integrity under hydroquinone-induced oxidative stress in a human iPSC-RPE/porcine neuroretina co-culture model
- biorxiv2026-08-17score 71metabolismredox biologysignaling
Alpha cells bank pentose-phosphate redox at higher glucose so glucagon still fires when sugar falls
Live-cell redox imaging in alpha cells inside intact islets shows that glucose flux through the pentose phosphate pathway raises cytosolic redox potential. That prior redox charge, not a simple low-glucose mitochondrial story, helps keep protein kinase A (PKA) on and glucagon available during hypoglycemia. Antioxidants and a 5 mM glucose pre-incubation manipulate the charge; whole-body redox state changes the mouse counterregulatory response. The authors explicitly ask whether non-mitochondrial glucose metabolism potentiates glucagon at low glucose.
Source preprint: Glucose derived redox equivalents preserve PKA activity and glucagon secretion during hypoglycaemia
- biorxiv2026-08-14score 70immunologymetabolismredox biology
Severe endometriosis lesion vesicles enter endothelial mitochondria and push angiogenesis
Small extracellular vesicles from endometriosis patients change with stage and source. Lesion-derived vesicles lose epithelial surface markers, gain immune signatures, and, when they come from severe disease, show enhanced uptake and mitochondrial localization in human uterine microvascular endothelial cells and promote angiogenesis. Plasma vesicles shift adhesion- and platelet-associated profiles. Multi-omics add coordinated immune, matrix, epithelial, vascular, oxidative-stress, and metabolic programs. The mitochondrial claim is trafficking-plus-function in endothelial cells, not a respiratory-chain map of the lesion.
Source preprint: Endometriosis patient-derived small extracellular vesicles carry unique immune, proteomic and lipidomic signatures associated with mild and severe endometriosis
- biorxiv2026-08-21score 68metabolismredox biologybioprocess
Late CHO fed-batch cells burn fat in mitochondria and peroxisomes, then flirt with ferroptosis
Across ambr250 CHO fed-batch conditions, cultures follow a conserved path: proliferate, transition, then a high-stress end state of mitochondrial and peroxisomal fatty-acid β-oxidation, lipid remodeling, oxidative burden, and ferroptosis-associated pathways. Richer feeds delay that switch via redox/glutathione defense but do not raise antibody titre in proportion. Survival spends the resources that would have been titer. Fatty-acid oxidation and ferroptosis are the late-stage constraints to engineer against.
Source preprint: Fatty Acid β-oxidation and Ferroptosis Define a Survival-Productivity Trade Off in CHO fed-Batch Bioreactors
- biorxiv2026-08-31score 61bioenergeticsinfectionredox biology
Phytophthora under PEG water limitation grows faster and turns alternative oxidase up
Five percent PEG-3350, a moderate water limit, speeds Phytophthora cinnamomi radial growth. A time-resolved proteome (1,097 groups) mostly falls; the few risers include thioredoxin/glutaredoxin and alternative oxidase. Adaptation looks like redox and mitochondrial metabolic regulation, not a crash stress response.
Source preprint: Osmotic adaptation rather than stress response: A time-resolved proteomic analysis of PEG-induced water limitation in Phytophthora cinnamomi