Pharmacology Research Center, Bio-organic Science Division, Korea Research Institute of Chemical Technology, Daejeon 305-600, Korea. yscho @krict.re.kr
Mol Cells. 2010 Apr;29(4):327-32. doi: 10.1007/s10059-010-0066-3.
Cell death occurs spontaneously or in response to external stimuli, and can be largely subdivided into apoptosis and necrosis by the distinct morphological and biochemical features. Unlike apoptosis, necrosis was recognized as the passive and unwanted cell demise committed in a non-regulated and disorganized manner. However, under specific conditions such as caspase intervention, necrosis has been proposed to be regulated in a well-orchestrated way as a backup mechanism of apoptosis. The term programmed necrosis has been coined to describe such an alternative cell death. Recently, at least some regulators governing programmed necrosis have been identified and demonstrated to be interconnected via a wide network of signal pathways by further extensive studies. There is growing evidence that programmed necrosis is not only associated with pathophysiological diseases, but also provides innate immune response to viral infection. Here, we will introduce recent updates on the molecular mechanism and physiological significance of programmed necrosis.
细胞死亡是自发发生的，或者是对外界刺激的反应，可以根据明显的形态和生化特征，主要分为细胞凋亡和细胞坏死。与细胞凋亡不同，细胞坏死被认为是一种非调控和无组织的被动的、不受欢迎的细胞死亡方式。然而，在特定条件下，如半胱氨酸天冬氨酸蛋白酶（caspase）的干预下，细胞坏死已经被提出以一种精心协调的方式被调控，作为细胞凋亡的备用机制。程序性细胞坏死这一术语被用来描述这种替代的细胞死亡。最近，通过进一步广泛的研究，至少已经确定了一些调控程序性细胞坏死的因子，并证明它们通过广泛的信号通路网络相互关联。越来越多的证据表明，程序性细胞坏死不仅与病理生理疾病有关，而且还为病毒感染提供先天免疫反应。在这里，我们将介绍程序性细胞坏死的分子机制和生理意义的最新进展。
