中文摘要：

细胞凋亡是一个受到一系列相关基因严格调控的细胞死亡过程。线粒体是细胞凋亡调控的活动中心。在凋亡因子的刺激下，线粒体释放出不同促凋亡因子如细胞色素C、Smac／Diablo等，激活细胞内凋亡蛋白酶Caspase。我们发现，活化后的Caspase可以反过来作用于线粒体，引发更大量线粒体细胞色素c的释放，构成细胞色素c释放的正反馈调节机制，从而导致电子传递链的中断、膜电势的丧失、胞内ROS的升高以及线粒体产生ATP功能的完全丧失。Bcl-2家族蛋白在细胞色素C释放和细胞凋亡调控中起关键作用。

英文摘要：

Apoptosis is a highly regulated form of programmed cell death, which plays a key role in the development and homeostasis of multicellular organisms. Mitochondria play a central role in the regulation of apoptotic cell death. Upon death stimuli, different apoptogenic factors such as cytochrome c and Smac/Diablo are released during the early stages of apoptosis. A small amount cytochrome c may be sufficient for activating caspases. Once activated, caspases can positively feedback to attack mitochondria leading to a more profound loss of cytochrome c and consequently mitochondrial dysfunction. This caspase-mediated late stage of cytochrome c release causes the complete disruption of mitochondrial electron transport chain, leading to the increase in cellular ROS and complete loss of ATP generation, late stage of apoptotic events or secondary necrosis. Bcl-2 and its family proteins are important for regulating cytochrome c release and apoptotic processes.