Jeong Seon-Yong, Seol Dai-Wu
Department of Medical Genetics, School of Medicine, Ajou University, Suwon, Korea.
BMB Rep. 2008 Jan 31;41(1):11-22. doi: 10.5483/bmbrep.2008.41.1.011.
Apoptosis (programmed cell death) is a cellular self-destruction mechanism that is essential for a variety of biological events, such as developmental sculpturing, tissue homeostasis, and the removal of unwanted cells. Mitochondria play a crucial role in regulating cell death. Ca2+ has long been recognized as a participant in apoptotic pathways. Mitochondria are known to modulate and synchronize Ca2+ signaling. Massive accumulation of Ca2+ in the mitochondria leads to apoptosis. The Ca2+ dynamics of ER and mitochondria appear to be modulated by the Bcl-2 family proteins, key factors involved in apoptosis. The number and morphology of mitochondria are precisely controlled through mitochondrial fusion and fission process by numerous mitochondria-shaping proteins. Mitochondrial fission accompanies apoptotic cell death and appears to be important for progression of the apoptotic pathway. Here, we highlight and discuss the role of mitochondrial calcium handling and mitochondrial fusion and fission machinery in apoptosis.
细胞凋亡（程序性细胞死亡）是一种细胞自我毁灭机制，对于多种生物学事件至关重要，如发育塑形、组织稳态维持以及清除不需要的细胞。线粒体在调节细胞死亡过程中起着关键作用。长期以来，钙离子一直被认为是凋亡途径的参与者。已知线粒体可调节和同步钙离子信号传导。线粒体中钙离子的大量积累会导致细胞凋亡。内质网和线粒体的钙离子动态似乎受到凋亡相关关键因子Bcl-2家族蛋白的调节。线粒体的数量和形态通过众多线粒体塑形蛋白参与的线粒体融合和裂变过程得到精确控制。线粒体裂变伴随着凋亡性细胞死亡，并且似乎对凋亡途径的进展很重要。在此，我们着重探讨线粒体钙处理以及线粒体融合和裂变机制在细胞凋亡中的作用。
