高血糖通过氧化应激诱发糖尿病视网膜病变  

Hyperglycemia induces diabetic retinopathy through oxidative stress

作　　者：丁玉婉 黄虹 许静[2] Ding Yuwan;Huang Hong;Xu Jing(Jining Medical University,Jining Shandong 272067,China;Department of Ophthalmology,Jining No.1 People's Hospital,Jining Shandong 272000,China)

机构地区：[1]济宁医学院,山东济宁272067 [2]济宁市第一人民医院眼科,山东济宁272000

出　　处：《国际眼科纵览》2023年第5期424-429,共6页International Review of Ophthalmology

摘　　要：糖尿病视网膜病变(diabetic retinopathy,DR)是糖尿病视网膜微血管并发症之一,其主要病理变化包括视网膜炎症、血管通透性增高和视网膜表面血管生成异常。多种机制均参与了DR的发展,氧化应激是其发展的一个重要机制,它包括多元醇途径、晚期糖基化终产物(advanced glycation end products,AGEs)途径、己糖胺途径(hexosamine pathway,HBP)、蛋白激酶C(protein kinase C,PKC)途径和血管紧张素II(angiotensin II,ANG II)通路等。氧化应激的启动会引发细胞内级联反应,产生过多的活性氧,过量的活性氧会导致蛋白质修饰、炎症反应、细胞凋亡、自噬失调、线粒体功能受损,干扰多种信号通路,影响多种生物学过程,导致DR的发生和进展。进一步研究这些相互作用对于理解DR的发病机制以及寻找相关治疗策略具有重要意义。Diabetic retinopathy(DR)is a retinal microvascular complication that arises with the prolongation of the disease in diabetic patients.Its main pathological changes include retinal inflammation,increased vascular permeability,and abnormal retinal surface angiogenesis.Multiple mechanisms are involved in the development of DR,and oxidative stress is an important mechanism in its development,which includes the polyol pathway,advanced glycation end products(AGEs)pathway,the hexosamine pathway(HBP),the protein kinase C(PKC)pathway,and the angiotensin II(ANG II)pathway.The initiation of oxidative stress triggers an intracellular cascade reaction that generates excessive reactive oxygen species.Excessive reactive oxygen species lead to protein modification,inflammatory response,apoptosis,dysregulation of autophagy,impaired mitochondrial function,interfering with a variety of signaling pathways and affecting a variety of biological processes,which result in the onset and progression of DR.Further study of these interactions is important for understanding the pathogenesis of DR and finding relevant therapeutic strategies.

关 键 词：糖尿病视网膜病变 炎症 氧化应激 

分 类 号：R587.2[医药卫生—内分泌] R774.1[医药卫生—内科学]