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Ca 2+ ‐Mediated Mitochondrial Dysfunction and the Protective Effects of Bcl‐2
Author(s) -
MURPHY ANNE N.
Publication year - 1999
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1999.tb07815.x
Subject(s) - excitotoxicity , microbiology and biotechnology , neurodegeneration , bioenergetics , programmed cell death , mitochondrion , apoptosis , homeostasis , chemistry , function (biology) , biology , medicine , biochemistry , disease
Mitochondrial Ca 2+ 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 Ca 2+ 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 Ca 2+ uptake capacity and resistance to Ca 2+ ‐induced damage is discussed in light of current information on apoptotic signaling pathways.