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Importance briefs on mitochondria preprints — free to read, x402 for research bots
We track mitochondria-related preprints on bioRxiv and medRxiv, then publish original importance briefs you can read free in the browser. Research bots use the same analysis as machine-readable JSON via x402.
Score on each brief = editorial importance 0–100 for mitochondria research (see Method).
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2026-09-07
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View all →- biorxiv2026-08-14score 94
POLG occipital epilepsy is an immunometabolic lesion: OXPHOS collapse meets innate inflammation in visual cortex
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 OXPHOS and interneuron proteins than frontal cortex — a baseline that may explain why status epilepticus detonates occipitally in this mitochondrial disease.
- biorxiv2026-08-26score 93
NLRX1 is the CypD-independent handle on the mitochondrial permeability transition pore
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 raises the calcium threshold for pore opening in CRISPR-edited human cells and Nlrx1-knockout mouse tissue, independently of cyclophilin D (CypD); the oral lead GSK900 is active in an mPTP-sensitive neurological injury model.
- biorxiv2026-08-13score 92
Past 70% mtDNA heteroplasmy, cells need pyruvate carboxylase — or exogenous asparagine — to keep translating
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 or pyruvate carboxylase overexpression. Respiration-deficient cells become asparagine auxotrophs when PC is low — and L-asparaginase shrinks a high-heteroplasmy, low-PC thyroid tumor model.
- biorxiv2026-08-12score 91
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.
- medrxiv2026-08-25score 90
251,512 biobank genomes already held mitochondrial DNA. This pipeline finally calls it.
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 12.9 million mitochondrial DNA variant observations across 251,512 people without new sequencing. The missing product was never the reads. It was a harmonized, heteroplasmy-aware call set that biobanks would actually ship.
- biorxiv2026-08-20score 89
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.
- biorxiv2026-08-19score 88
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.
- biorxiv2026-08-15score 88
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.
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