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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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188
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2026-10-02
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View all →Sorted by importance score, then posted date — not recency.
- biorxiv2026-09-08score 94
A TYMP mRNA-lipid nanoparticle resets blood nucleosides in a mitochondrial DNA depletion syndrome within hours
Mitochondrial neurogastrointestinal encephalomyopathy is a thymidine-phosphorylase failure that poisons mitochondrial nucleotide pools systemically. Intravenous human TYMP mRNA in lipid nanoparticles puts the enzyme in mouse liver, is tolerated, and returns circulating nucleosides to wild-type in hours for up to three weeks at 0.25 mg/kg. Subcutaneous dosing works if you add hyaluronidase.
- 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.
- biorxiv2026-09-30score 93
Gasdermin E pores the mitochondrial inner membrane and lets apoptotic mitochondrial DNA out
The cleaved N-terminus of Gasdermin E assembles cardiolipin-preferring pores in the mitochondrial inner membrane during apoptosis, before the plasma membrane fails. Losing Gasdermin E cuts cristae swelling, inner-membrane extrusion, mitochondrial DNA release, and stimulator of interferon genes (STING) inflammation when caspases are blocked.
- biorxiv2026-09-07score 93
Cryo-EM shows Complex III does not assemble the two protomers in parallel, and CIII2CIV is born during that assembly
The textbook stepwise, symmetric assembly of dimeric mitochondrial Complex III is wrong in the cryo-EM intermediates. Subunit incorporation can uncouple from folding (cytochrome c1), and after dimerization the two protomers do not mature in lockstep (intermembrane-space domain). Non-vertebrate supercomplex CIII2CIV forms on that same assembly path, which favors cooperative supercomplex birth over late docking of finished complexes.
- 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.
- biorxiv2026-09-06score 92
Raptinal does not punch mitochondria; it jams folding, then TIM23 import permeabilizes the organelle
Proteostasis failure can kill mitochondria without BAX and BAK. Raptinal, the textbook fast apoptotic, is shown here as a folding poison. Misfolded new proteins flood import, the outer membrane opens, and VBIT4 plus TIM23-PAM blockade stop that death without touching canonical BAX-BAK apoptosis. Import flux is the fuse between a broken cytosol and a leaky organelle.
- biorxiv2026-09-03score 92
Lysosomes hand Fe(II) to mitochondria at contact sites, skipping mitoferrins and the cytosol
The textbook says mitochondria drink ferrous iron from the cytosolic labile pool through MFRN transporters. Live structured-illumination microscopy here shows Fe(II) crossing mitochondria-lysosome contacts on a PPS39/TOMM22/SFXN1 path that bypasses that pool. SFXN1 knockdown drops mitochondrial Fe(II) even when you ignore its serine job. Lysosomes are not just storage. They are a direct iron dock.
- 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.
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