细胞色素C、线粒体与凋亡

线粒体细胞色素C释放在细胞凋亡过程中起重要作用。细胞色素C释放到胞质后可引发caspase活化级联 ,导致细胞死亡。细胞色素C的释放是线粒体外膜通透性增高的结果。Bcl 2蛋白家族具有调控细胞色素C释放的功能。除细胞色素C外 ,线粒体膜间隙的凋亡诱导因子 (AIF)在凋亡过程中也释放至胞质 ,这两种途径充分保证了细胞死亡程序的有效执行。轻中度暂时性脑缺血后细胞色素C释放至胞质 ,早于DNA片段化

Cytochrome C、mitochondria and apoptosis

There is an evidence that mitochondrial cytochrome C has dual functions in controlling both cellular energetic metabolism and apoptosis. Once released, cytochrome C, in interaction with apoptotic protease activating factors (Apaf 1), initiates the activation of the execution caspases that lead to the subsequent apoptosis. Release of cytochrome C is the result of a perturbation of mitochondrial membrane permeability. Anti apoptotic Bcl 2 family proteins function as gatekeepers to prevent the release of cytochrome C. In addition to cytochrome C, mitochondria release other apoptogenic proteins including apoptosis inducing factor (AIF) during apoptosis. These two pathways may work together to induce complete apoptosis. After transient cerebral ischemia, the release of cytochrome C occurs from mitochondria, preceding DNA fragmentation.