Apoptosis normally proceeds in an orderly manner as part of natural cell turnover and development, but that's not the only path to death. A quick influx of calcium ions, or extreme oxidative stress, as happens in cases of stroke, heart attack, or other ischemic events, can cause mitochondria to swell and burst, releasing necrotic mediators. The path that cells take appears intimately linked with the permeability of mitochondrial membranes.
Four groups, publishing in 2005, independently showed that the mitochondrial protein cyclophilin D (CyPD) can mediate the transition to mitochondrial permeability that leads to necrotic cell death.1-4 Two of these papers have been cited more than 100 times each.1, 2 The studies offered insight into the regulation of cell-death decisions and established a key protein that works with the long-sought after permeability pore. Though the findings haven't exposed the structure of the pore or pieced together its exact mechanism of action, ...
