Mitochondrial calcium handling during ischemia-induced cell death in neurons

摘要

Mitochondria sense and shape cytosolic Ca~(2+) signals by taking up and subsequently releasing Ca~(2+) ions during physiological and pathological Ca~(2+) elevations. Sustained elevations in the mitochondrial matrix Ca~(2+) concentration are increasingly recognized as a defining feature of the intracellular cascade of lethal events that occur in neurons during cerebral ischemia. Here, we review the recently identified transport proteins that mediate the fluxes of Ca~(2+) across mitochondria and discuss the implication of the permeability transition pore in decoding the abnormally sustained mitochondrial Ca~(2+) elevations that occur during cerebral ischemia.