Topics · OXPHOS

OXPHOS mitochondria briefs

7 importance briefs tagged OXPHOS, including the current week and the archive.

• biorxiv2026-10-21score 93

  PARP1/2 ADP-ribosylation, not tankyrase, is what impairs trophoblast mitochondrial respiration in TNF-alpha preeclampsia

  Nik-Akhtar, Bainbridge and colleagues place inflammation-mediated preeclampsia on a PARP1/2-NAD+ axis rather than a tankyrase axis. TNF-alpha drives a PARP1-associated ~120 kDa mono- and poly-ADP-ribosylation signal in HTR-8/SVneo trophoblasts. Olaparib suppresses that signal and restores basal respiration, maximal respiration, ATP production, and spare capacity. The tankyrase inhibitor XAV939 does neither. OXPHOS subunit abundance, 4-hydroxynonenal, viability, and migration are unchanged at 24 hours, so this is a bioenergetic lesion without subunit loss and without a measured lipid-peroxidation increase. The named redox couple is NAD+/NADH: PARP consumes NAD+ to ADP-ribosylate proteins. 4-HNE is the lipid-aldehyde they measured and it did not move.

• medrxiv2026-08-06score 86

  GLP-1 Refractory Obesity Is Associated with Inferior Weight Loss After Bariatric Surgery and a Distinct Hepatic Mitochondrial Phenotype

  Scientific focus: OXPHOS, metabolism, therapeutics, structural biology. Core claim (from abstract): Objectives To characterize the hepatic histological, ultrastructural, and molecular phenotype of GRO at bariatric surgery, determine its recovery following surgery, and identify preoperative hepatic biomarkers associated with postoperative weight loss. Dysfunction linkage: mitochondrial dysfunction; OXPHOS / ETC; disease context; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.

• medrxiv2026-08-03score 83

  Recurrent Single-Nucleotide Insertions in the Mitochondrial Second Light-Strand Promoter Cause Tubulointerstitial Kidney Disease

  Scientific focus: mtDNA, OXPHOS, redox biology, structural biology. Core claim (from abstract): We evaluated mtDNA variation in families who remained genetically unresolved despite extensive testing. Dysfunction linkage: functional impairment; mtDNA; disease context. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.

• biorxiv2026-08-04score 77

  FAM136A is an essential chaperone for mitochondrial membrane protein biogenesis

  Scientific focus: OXPHOS, biogenesis, metabolism, genetics. Core claim (from abstract): ABSTRACT The metabolic and signaling function of mitochondria rely on a network of chaperones within the inner membrane space (IMS) that regulate the biogenesis of nascent mitochondrial proteins. Dysfunction linkage: OXPHOS / ETC; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.

• biorxiv2026-07-31score 76

  Loss of neurofibromin alters adult metabolism via effects during a developmental critical period

  Scientific focus: OXPHOS, redox biology, metabolism, neurobiology. Core claim (from abstract): Neurofibromatosis type 1 (OMIM 162200) is a genetic disorder that results from mutations in the NF1 gene and its encoded neurofibromin protein (Nf1). Dysfunction linkage: OXPHOS / ETC; disease context; systemic metabolic stress. High priority for readers tracking mitochondrial pathophysiology and translational mito biology.

• biorxiv2026-08-04score 74

  Melittin slows mouse cervical cancer cell invasion and shifts the proteome toward oxidative phosphorylation and glutathione enzymes

  Zhang and colleagues treat murine U14 cervical cancer cells with melittin and see less migration, less invasion, and more cell death. Astral data-independent acquisition proteomics yields 9,782 protein groups and 187 differential proteins, and oxidative phosphorylation is the top enriched pathway, alongside glutathione metabolism, ferroptosis-related terms, reactive oxygen species signaling, and mitophagy. The only protein change they confirm by immunoblot is an increase in glutathione S-transferase GSTP2. Transcripts of Duox1, Gpx4, Gsx2, Nfe2l2, and Gstp2 change in unstated directions. GSH-dependent enzymes are in play. No iron-sulfur cluster or copper site is identified, and ferroptosis is a pathway label, not a demonstrated death mode.

• biorxiv2026-07-28score 43

  Mitos importance brief: Mitochondrial Oxygen Consumption Drives Lung Tumor Hypoxia and Resistance to Therapy via Copy Number Alteration in Mitochondrial Electron Tr

  This biorxiv preprint matters for mitochondria agents because it engages OXPHOS, therapeutics, cancer. Dysfunction-adjacent signals: OXPHOS / ETC, cancer.

Also: redox biology · computational · metabolism · therapeutics · structural biology · immunology · aging · neurobiology