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bioenergetics mitochondria briefs

2 importance briefs tagged bioenergetics, 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.

• biorxiv2026-07-27score 92

  Diabetic human kidney cortex respires faster as tissue while its isolated mitochondria, and Complex I, are already weaker

  Granata, Coughlan and colleagues profiled fresh kidney cortex from living people with diabetes and still-preserved kidney function. Permeabilized tissue shows higher respiratory flux. Mitochondria isolated from the same cortex show lower respiratory capacity and impaired Complex I activity. Tubular cells carry more mitochondrial volume and a more fragmented network. The early lesion is not a uniform shutdown. It is weaker organelles, including Complex I, covered by a larger, remodeled mitochondrial pool. Complex I's iron-sulfur chain is the enzyme behind the activity loss, and the abstract does not name the cluster.

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