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

被引：31

作者：

Murphy, AN ^{[1
]}

机构：

[1] MitoKor, San Diego, CA 92121 USA

来源：

OXIDATIVE/ENERGY METABOLISM IN NEURODEGENERATIVE DISORDERS | 1999年 / 893卷

关键词：

D O I：

10.1111/j.1749-6632.1999.tb07815.x

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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.

引用

页码：19 / 32

页数：14