In diabetic retinopathy, a calcium channel called TRPM7 drives VDAC1 up and forces open the mitochondrial pore in retinal cells

A team at Southwest Medical University in Luzhou, China, led by Ping Liu and Dongchuan Zuo, was digging into why chronically high blood sugar damages the retina, specifically the Muller cells that support and nourish retinal neurons. They traced the chain back to a calcium channel called TRPM7, which gets switched on by high glucose and lets a sustained flood of calcium into the cell.

That calcium surge did something specific: it pushed up expression of VDAC1 and helped force open the mitochondrial permeability transition pore, the same kind of large, leaky opening that shows up across so many VDAC1-linked diseases on this site. The result was collapsed mitochondrial membrane potential, ATP depletion, oxidative stress, and cell death. Silencing TRPM7 reversed all of it, calcium levels dropped, VDAC1 came back down, and the mitochondria stayed intact.

It is a tidy addition to the VDAC1 disease map, a calcium channel most people have never heard of turns out to be one lever upstream of VDAC1-driven mitochondrial collapse, this time in the eye.