脑缺血过程中自噬作用的研究进展  

The Research Progress of Autophagy in Cerebral Ischemia

作　　者：陈颖霞[1] 汤永红[1] 

机构地区：[1]南华大学附属第二医院神经内科,湖南省衡阳市421001

出　　处：《中国动脉硬化杂志》2016年第6期644-648,共5页Chinese Journal of Arteriosclerosis

摘　　要：缺血性脑卒中是致死致残率极高的一类难治性疾病。越来越多的证据表明,适度的自噬可以清除受损细胞器,从而保护细胞抵御各种伤害;然而,长期过度自噬,使得细胞内容物降解过多引发细胞死亡,导致组织器官严重损伤。在多个不同的缺血性脑损伤动物模型中观察到,缺血性脑损伤过程中自噬被激活并参与其神经元死亡的调节。本文就缺血性脑损伤过程中自噬的相关作用的研究进展做一概述。Ischemic storke is a kind of intractable disease with high mortality and disability. There is increasing evidence that a moderate autophay can clean damaged organelles,so as to protect cells against damage. However,excessive autophagy can degrade cell components too much to induce cell death and serious injury of tissues and organs. In a number of different animal models with hypoxic-ischemic brain injury,autophagy is activated and involves regulating neuronal death in the processes of cerebral ischemic injury. In this paper,we summarize the fucntion of autophay in ischemic brain injury.

关 键 词：自噬 脑缺血损伤 神经元死亡 

分 类 号：R741[医药卫生—神经病学与精神病学]