Murphy A N
MitoKor, San Diego, California 92121, USA.
Ann N Y Acad Sci. 1999;893:19-32. doi: 10.1111/j.1749-6632.1999.tb07815.x.
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.
线粒体对钙离子的摄取可能在兴奋性毒性和缺血再灌注损伤中导致细胞死亡，并且也可能参与慢性神经退行性变，其中生物能量功能的损害会改变细胞内钙离子的稳态。已知Bcl-2过表达可防止钙离子介导的死亡；其保护机制仍未明确。我们根据目前有关凋亡信号通路的信息，讨论了Bcl-2增强线粒体摄取钙离子能力以及抵抗钙离子诱导损伤能力的数据。
