Tait S W G, Green D R
Department of Immunology, St Jude Children's Research Hospital, Memphis, TN 38105, USA.
Oncogene. 2008 Oct 27;27(50):6452-61. doi: 10.1038/onc.2008.311.
Apoptosis is dependent upon caspase activation leading to substrate cleavage and, ultimately, cell death. Although required for the apoptotic phenotype, it has become apparent that cells frequently die even when caspase function is blocked. This process, termed caspase-independent cell death (CICD), occurs in response to most intrinsic apoptotic cues, provided that mitochondrial outer membrane permeabilization has occurred. Death receptor ligation can also trigger a form of CICD termed necroptosis. In this review, we will examine the molecular mechanisms governing CICD, highlight recent findings demonstrating recovery from conditions of CICD and discuss potential pathophysiological functions of these processes.
细胞凋亡依赖于半胱天冬酶的激活，这会导致底物裂解，并最终导致细胞死亡。尽管半胱天冬酶的激活是细胞凋亡表型所必需的，但很明显，即使半胱天冬酶功能被阻断，细胞也常常会死亡。这个过程被称为半胱天冬酶非依赖性细胞死亡（CICD），在大多数内源性凋亡信号的作用下都会发生，前提是线粒体外膜通透性已经发生改变。死亡受体连接也可触发一种称为坏死性凋亡的CICD形式。在这篇综述中，我们将研究控制CICD的分子机制，强调最近表明从CICD状态恢复的研究结果，并讨论这些过程潜在的病理生理功能。
