Ca2+-mediated mitochondrial dysfunction and the protective effects of Bcl-2

Mitochondrial Ca2+ sequestration likely contributes to cell death in excitotoxicity and ischemia reperfusion injury, and may also be involved in chronic forms of neurodegeneration in which a compromise in bioenergetic function alters cellular Ca2+ homeostasis. Bcl-2 overexpression is known to protect against Ca2+-mediated death; the mechanism of protection remains unresolved. Our data of the ability of Bcl-2 to potentiate mitochondrial Ca2+ uptake capacity and resistance to Ca2+-induced damage is discussed in light of current information on apoptotic signaling pathways.