Ca2+-mediated mitochondrial dysfunction and the protective effects of Bcl-2
Ca2+-mediated mitochondrial dysfunction and the protective effects of Bcl-2
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DOI：
10.1111/j.1749-6632.1999.tb07815.x
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发表时间：
1999-01-01
期刊：
影响因子：
--
通讯作者：
Murphy, AN
中科院分区：
文献类型：
--
作者：
Murphy, AN
线粒体Ca 2+螯合可能导致兴奋性毒性和缺血再灌注损伤中的细胞死亡，并且还可能参与慢性形式的神经变性，其中生物能量功能的妥协改变了细胞Ca 2+稳态。已知Bcl-2过表达可防止Ca 2+介导的死亡;保护机制尚未解决。我们的数据Bcl-2的能力，以增强线粒体钙的摄取能力和抵抗钙离子诱导的损伤进行了讨论，在目前的信息凋亡信号通路。
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.