氧化应激与自噬在糖尿病血管并发症中的相互作用  

The action of autophagy and reactive oxygen species in the vascular complications of diabetes

作　　者：刘佳琦[1] 张伟华[1] 

机构地区：[1]哈尔滨医科大学基础医学院病理生理学教研室,黑龙江哈尔滨150081

出　　处：《解剖科学进展》2016年第4期436-438,共3页Progress of Anatomical Sciences

基　　金：国家自然科学基金(81370421)

摘　　要：血管损伤是糖尿病患者的常见并发症,血管内皮细胞的功能障碍是导致糖尿病血管损伤的主要危险因素。自噬是正常细胞在生长周期中必不可少的维持体内稳态的生理过程,其主要功能是细胞器回收和蛋白质的降解,异常自噬的发生将导致细胞线粒体的损伤并进而促进细胞死亡。内皮细胞线粒体是活性氧(ROS)产生的主要部位,糖尿病引起的高糖血症使细胞氧化应激水平升高,ROS产生增加,导致血管内皮细胞功能障碍。ROS可诱导细胞过度自噬,使内皮细胞发生凋亡与坏死,从而引起血管损伤。本文将对ROS及其诱导的过度自噬在促进糖尿病血管并发症中的病理生理作用和研究作一综述。Vascular injury is a common complication of diabetes, vascular endothelial cell dysfunction is a major cause of diabetes risk factors. Autophagy, it is essential to maintain the homeostasis of physiological processes in normal cell growth cycle, and its main function is to recycle organelles and protein degradation. Abnormal autophagy will lead to mitochondrial damage and thereby promote cell death. Endothelial cell mitochondria are the main parts of the reactive oxygen species（ROS） generation, hyperglycemia is caused by diabetes and increased levels of oxidative stress, then ROS generation increased, leading to endothelial cell dysfunction. ROS can induce excessive autophagy, leading to endothelial cell apoptosis and necrosis, thus causing vascular injury.The review will introduce ROS induced excessive autophagy in promoting diabetic vascular complications and its pathophysiological role.

关 键 词：氧化应激 自噬 血管损伤 体内稳态 内皮细胞 高糖血症 胰岛素抵抗 病理生理作用 细胞线粒体 活性氧 

分 类 号：R587.11[医药卫生—内分泌]