Ca(2+)-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 Ca(2+)-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 Ca(2+)-induced damage is discussed in light of current information on apoptotic signaling pathways.
Murphy
A N
AN
MitoKor, San Diego, California 92121, USA. murphya@mitokor.com
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D016923:Cell Death; D006706:Homeostasis; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D009410:Nerve Degeneration / Q000473:pathology / Q000503:physiopathology*; D009474:Neurons / Q000166:cytology / Q000473:pathology / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism*; D015427:Reperfusion Injury / Q000503:physiopathology
D019253:Proto-Oncogene Proteins c-bcl-2; D002118:Calcium