细胞凋亡综合信号通路图

摘要：
细胞凋亡是指为维持内环境稳定，由基因控制的细胞自主的有序的死亡。细胞凋亡与细胞坏死不同，细胞凋亡不是一件被动的过程，而是主动过程，它涉及一系列基因的激活、表达以及调控等的作用，它并不是病理条件下，自体损伤的一种现象，而是为更好地适应生存环境而主动争取的一种死亡过程。如图：

细胞凋亡是指为维持内环境稳定，由基因控制的细胞自主的有序的死亡。细胞凋亡与细胞坏死不同，细胞凋亡不是一件被动的过程，而是主动过程，它涉及一系列基因的激活、表达以及调控等的作用，它并不是病理条件下，自体损伤的一种现象，而是为更好地适应生存环境而主动争取的一种死亡过程。

细胞凋亡的过程大致可分为以下几个阶段：接受凋亡信号→凋亡调控分子间的相互作用→蛋白水解酶的活化(Caspase)→进入连续反应过程。

Apoptosis, or programmed cell death, is a regulated physiological process leading to cell death characterized by cell shrinkage, membrane blebbing and DNA fragmentation. Caspases, a family of cysteine proteases, are central regulators of apoptosis. Initiator caspases (including 8, 9, 10 and 12) are closely coupled to pro-apototic signals. Once activated, these caspases cleave and activate downstream effector caspases (including 3, 6 and 7) which in turn cleave cytoskeletal and nuclear proteins and induce apoptosis. Cytochrome C released from mitochondria is coupled to the activation of caspase 9, a key initiator caspase. Pro-apoptotic stimuli include the FasL, TNF, DNA damage and ER stress. Fas and the TNFR activate caspases 8 and 10; DNA damage leads to the activation of caspase 9; and ER stress leads to the calcium-mediated activation of caspase 12. Anti-apoptotic ligands including growth factors and cytokines activate AKT and p90RSK, which inhibit Bad and prevent cytochrome C release. TNFR can also stimulate an anti-apoptotic pathway by inducing IAP, which directly inhibits caspases 3, 7 and 9.