Mitochondrial regulation of apoptotic cell death
Mitochondrial regulation of apoptotic cell death
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DOI：
10.1016/j.cbi.2006.04.010
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发表时间：
2006-10-27
影响因子：
5.1
通讯作者：
Orrenius, Sten
中科院分区：
文献类型：
--
作者：
Gogvadze, Vladimir;Orrenius, Sten
线粒体在调节细胞凋亡和坏死性细胞死亡中起决定性作用。线粒体外膜的透化和随后的膜间空间蛋白的释放是两种细胞死亡模型的重要特征。这些蛋白质释放的机制可能取决于细胞类型和刺激的性质。在所涉及的机制中，线粒体通透性转换似乎主要与坏死相关，而在早期凋亡过程中caspase激活蛋白的释放主要由Bcl-2蛋白家族调节。然而，有越来越多的证据表明，这两种机制之间的相互作用和合作。线粒体透化的多种机制可以解释不同类型细胞中线粒体对许多凋亡刺激的反应中的不稳定性。(c)2006年由Elsevier爱尔兰有限公司出版。
Mitochondria play a decisive role in the regulation of both apoptotic and necrotic cell death. Permeabilization of the outer mitochondrial membrane and subsequent release of intermembrane space proteins are important features of both models of cell death. The mechanisms by which these proteins are released depend presumably on cell type and the nature of stimuli. Of the mechanisms involved, mitochondrial permeability transition appears to be associated mainly with necrosis, whereas the release of caspase activating proteins during early apoptosis is regulated primarily by the Bcl-2 family of proteins. However, there is increasing evidence for interaction and co-operation between these two mechanisms. The multiple mechanisms of mitochondrial permeabilization may explain diversities in the response of mitochondria to numerous apoptotic stimuli in different types of cells. (c) 2006 Published by Elsevier Ireland Ltd.