Mitochondrial Health Ratings
87 interventions, foods, drugs, supplements and lifestyle pillars like sleep, exercise, fasting, sauna and light, each graded for evidence, benefit and safety, and linked to the research. The honest, filterable database I wish existed. This is the one to start with.
Explore the ratings →graded
01Everything else, at a glance
Everything here in one glance, pick a door. New? The 5-minute VDAC1 primer is the gentlest start.
Research News
Recent mitochondria & VDAC1 research in plain words, always linked to the source.
Mito-Medicine Companies
A filterable watchlist of who's actually building mitochondrial medicine.
Clinical Trials
Mito-drug trials linked straight to their ClinicalTrials.gov records.
The VDAC1 Gene & Expression
The gene, its 283-amino-acid protein, and where in the body it's switched on.
VDAC1 Disease Body Map
Where VDAC1 goes wrong across the body, each organ linked to a key paper.
VDAC1 & Mitochondria Resources
The reviews, databases and labs I keep coming back to.
About me
PSEN1 carrier, x-tosis co-founder, and why this whole site exists.
02Fresh off the notebook
The latest bits. Full archive lives in news.
In septic T cells, VDAC1 oligomers open a pore that leaks mtDNA and drives inflammation, and VBIT-12 shuts it down
A Shanghai team watched VDAC1 clump up, leak mtDNA, and trip the cGAS–STING alarm in immune cells, and calmed the whole thing down with the oligomerization blocker VBIT-12.
the full story →→ Ren et al., Cell Signalling 2026 · doi.org/10.1016/j.cellsig.2026.112642
Losing the mitochondrial quality-control genes HtrA2 or PINK1 makes cells more likely to turn senescent after DNA damage
A De Montfort University team knocked out three separate mitochondrial quality-control genes in mouse cells and found that losing HtrA2 or the mitophagy regulator PINK1 made cells noticeably more prone to senescence after DNA-damaging drugs, while the DNA damage response itself didn't fully explain which cells actually became senescent.
read →In diabetic retinopathy, a calcium channel called TRPM7 drives VDAC1 up and forces open the mitochondrial pore in retinal cells
A Southwest Medical University team traced hyperglycemia-driven damage in retinal Muller cells to a calcium channel, TRPM7, that pushes VDAC1 expression up and forces open the mitochondrial permeability pore, and silencing TRPM7 protected the cells.
read →03VDAC1 in 3D
The actual crystal structure of human VDAC1 (PDB 2JK4), grab it and spin. Nineteen β-strands rolled into a barrel, N-terminal helix tucked inside. (Needs internet to load the atoms.)