论文部分内容阅读
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 in patients with diabetes, and dysfunction of vascular endothelial cells is a major risk factor for vascular damage in diabetic patients. Autophagy is essential for normal cells in the growth cycle to maintain the homeostasis of the physiological processes, its main function is the recovery of organelles and protein degradation, the occurrence of abnormal autophagy will lead to mitochondrial cell damage and thus promote cell death. Endothelial cell mitochondria are the main part of reactive oxygen species (ROS). Hyperglycemia caused by diabetes increases the level of oxidative stress in cells and ROS production, leading to dysfunction of vascular endothelial cells. ROS can induce excessive autophagy, causing apoptosis and necrosis of endothelial cells, leading to vascular injury. This article will review the pathophysiological role of ROS and its induced over-autophagy in the promotion of diabetic vascular complications.