糖尿病视网膜病变中周细胞功能异常的分子调控机制研究进展  

Abnormal molecular regulation mechanism of pericytes in diabetic retinopathy

作　　者：刘畅[1] 杨红[1] 曹国凡[1] 

机构地区：[1]南京医科大学附属眼科医院,210029

出　　处：《国际眼科纵览》2017年第5期300-305,共6页International Review of Ophthalmology

摘　　要：糖尿病视网膜病变（diabetic retinopathy,DR）是导致视功能障碍和视力丧失的主要原因之一,其发病机制复杂,涉及多种细胞、分子,至今尚未完全阐明.DR的主要病理特点是微血管功能紊乱,其中周细胞凋亡是DR的重要标志.周细胞凋亡的主要原因包括高血糖引起的活性氧和糖基化终产物的产生增加,血小板衍生生长因子表达下降,血管生成素2和转化生长因子β的上调以及色素上皮衍生因子水平降低等.近年来,关于糖尿病视网膜微血管病变中周细胞分子调控机制的研究取得很大突破.因此,本文对DR中周细胞功能异常和其分子调控机制做一综述,为防治糖尿病视网膜微血管病变的发生提供新的理论基础.Diabetic retinopathy （DR） is one of the leading causes of visual impairment and loss of vision.Its pathogenesis is complex and involves a variety of cells,molecules that have not yet been fully elucidated.The main pathological features of DR are microvascular dysfunction,in which pericyte loss is an important indicator of DR.The main reasons of pericyte loss include increased production of reactive oxygen species and advanced glycation end products,decreased expression of platelet-derived growth factor,the upregulation of angiopoietin2 and transforming growth factor β and the decrease of pigment epithelium-derived factor.In recent years,great breakthroughs have made on the molecular regulation mechanism of pericytes.This article tried to review the abnormal molecular regulation mechanism of pericytes,which was helpful to the treatment of diabetes and diabetic retinopathy.

关 键 词：糖尿病视网膜病变 周细胞 异常的分子调控机制 

分 类 号：R587.2[医药卫生—内分泌]