摘要
糖尿病是威胁人类健康的重要疾病,可引起血管内皮代谢紊乱和结构异常,导致机体心、脑、肾及视网膜等重要器官损伤。氧化应激是糖尿病血管内皮损伤的上游机制,目前还未完全明确。本文主要从高糖状态下自由基的形成和自由基通过晚期糖基化终产物、多元醇通路、蛋白激酶激活和己糖胺合成通路激活等路径介导的血管内皮细胞氧化损伤进行综述,为临床防治糖尿病提供依据。
Diabetes is recognized as a worldwide health crisis which causes vascular endothelial damage and damage to multiple organs heart,brain,kidney and retina,leading to various complications. Oxidative stress has been suggested to be a common upstream event for the pathogenesis of these complications, but the mechanisms need to be explored further. Compelling evidence has been provided that biochemical mechanisms involved in hyperglycemia induced vascular endothelial dysfunction are associated with the generation of free radicals and the activation of 4 major pathways mediated by free radicals： polyol pathway flux,increased formation of AGEs,activation of protein kinase C isoforms,and overactivity of the hexosamine pathway. This review presents a summary of our current understanding of vascular damage in diabetes induced by oxidative stress to shed a novel light on diabetes management for health care system.
出处
《齐齐哈尔医学院学报》
2015年第10期1494-1496,共3页
Journal of Qiqihar Medical University
基金
广州市科技攻关项目(201300000157)
关键词
糖尿病
血管内皮细胞
氧化应激
Diabetes
Vascular endothelial damage
Oxidative stress
