Archive · 2026-W42

Mito.news 2026-W42

6 articles. Each URL is the original /articles/{id} path.

• 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.

• biorxiv2026-08-04score 91

  Cholesterol in APOE4 astrocytes truncates cristae, drops Complexes I and IV, and leaves cells dependent on a reversing ATP synthase

  Lee, Holt and colleagues find that APOE4 mouse astrocytes with high intracellular cholesterol build sparse, truncated cristae and extra crista-junction complexes, lose respiratory Complexes I and IV, and respire less. Membrane potential still rises, because proton leak is low and ATP synthase runs in reverse, hydrolyzing ATP to support the gradient. Oligomycin becomes selectively toxic, and sequestering cholesterol with methyl-β-cyclodextrin removes that toxicity. The lost complexes imply iron-sulfur, heme, and copper sites. The abstract reports the complexes, not the metals. The enzyme they actually catch misbehaving is ATP synthase.

• biorxiv2026-07-29score 86

  Ringer loss weakens fruit-fly Complex I, raises superoxide, and matches a Complex I deficit in Parkinson disease brain

  Tillmon and colleagues place Ringer, the Drosophila homolog of human tubulin polymerization promoting protein (TPPP), in the mitochondrial matrix and show that losing it lowers Complex I subunits, assembly factors, and enzymatic activity. The oxygen species they measure is superoxide. Complex I moves electrons from NADH through FMN into a chain of iron-sulfur clusters and out to ubiquinone at cluster N2, but this abstract never names which cluster or which core oxidation level failed. The Parkinson link is real as a claim and thin as a dataset: they say postmortem human brain shows similar deficits, without listing the human subunits.

• biorxiv2026-08-04score 80

  Black carbon holds immune cells in an OMA1-DELE1 stress response; ultrafine particles and nanoplastics take shorter paths

  In human peripheral blood mononuclear cells, ultrafine particulate matter, black carbon, and polystyrene nanoplastics all move oxidative stress and mitochondrial markers, but not on the same clock. Ultrafine particles look acute and adaptive. Black carbon looks chronic, with a persistent OMA1-DELE1 integrated stress response and inflammation. Polystyrene nanoplastics sit in between: lower, longer adaptation plus biogenesis. ND1 and Complexes I through V are expression markers here, not measured iron-sulfur or copper centers. OMA1's metal is also unnamed.

• biorxiv2026-07-28score 76

  Corilagin saves glutathione, membrane potential, and the AMPK-TFAM axis in high-glucose neuroblastoma cells

  In SH-SY5Y cells, 50 mM glucose for 24 hours depletes reduced glutathione, raises intracellular and mitochondrial reactive oxygen species, drops membrane potential, fragments the network, and increases cell death. Corilagin pretreatment opposes each of those changes and restores AMPK phosphorylation plus SIRT1, PGC-1α, and TFAM. The named redox species is reduced glutathione, one side of the GSH/GSSG couple. No metal site is identified. The abstract's wider disease framing (diabetic nephropathy, cerebral ischemia) is not the experiment it describes.

• 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.