自噬在脑缺血性损伤中的作用

Effects of autophagy in cerebral ischemic injury

自噬是一种细胞内成分自我降解的过程,包括自噬的诱导、自噬体膜的形成、自噬体的形成、自噬体与溶酶体的融合以及内容物的降解。自噬若适度激活,则促进细胞存活;若过度激活,则可加重细胞损伤,甚至导致细胞裂解和促进细胞死亡。该文主要从自噬的形成过程及分子机制、脑缺血后自噬的诱发因素、自噬参与脑缺血的信号转导通路及自噬在脑缺血损伤中的作用进行综述,为进一步研究自噬与脑缺血性损伤及其药物调控提供参考。

Autophagy, a process of intracellular component deg- radation, consists of initiation, vesicle membrane, vesicle ex- pansion and completion, vesicle fusion and autophagosome deg- radation. Moderate activation of autophagy may promote cell sur- vival, while excessive activation of autophagy may aggravate cell injury, or even lead to cell lysis and death. This paper mainly reviews the process and the molecular basis of autophagy, as wellas trigger factors, signal transduction pathways involved in cere- bral ischemia, along with its effects on ischemic brain injury, which will provide a reference for further probe of autophagy in cerebral ischemic injury and its drug regulation.