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糖尿病性视网膜病变分子机制的研究进展
引用本文:崔彦,许迅. 糖尿病性视网膜病变分子机制的研究进展[J]. 眼视光学杂志, 2007, 9(2): 135-138
作者姓名:崔彦  许迅
作者单位:1. 上海市第一人民医院眼科,上海,200080;济南施尔明眼科医院,山东,济南,250021
2. 上海市第一人民医院眼科,上海,200080
摘    要:糖尿病性视网膜病变是发达国家首位的致盲原因,慢性高血糖是其主要原因。对于高血糖导致糖尿病性视网膜病变的生化和分子机制,目前有五种假说:多元醇途径的增加、终末糖基化产物的增加、蛋白激酶C的激活、增加的己糖胺途径以及线粒体活性氧产生增多。本文对各途径的分子机制研究进展予以综述,并分析各途径间的相互关联及将来的研究方向。

关 键 词:糖尿病/并发症  糖尿病视网膜病变/病因学  分子生物学  生物化学
文章编号:1008-1801(2007)02-0135-04
修稿时间:2006-03-12

Molecular mechanism of diabetic retinopathy
CUI Yan,XU Xun. Molecular mechanism of diabetic retinopathy[J]. Chinese Journal of Optometry & Ophthalmology, 2007, 9(2): 135-138
Authors:CUI Yan  XU Xun
Abstract:Diabetic retinopathy is the leading cause of blindness in developed countries. Chronic hyperglycemia has an important role in the pathogenesis of this complication. There are five hypotheses for the biochemistry and molecular biology mechanisms of diabetic retinopathy induced by hyperglycemia. These hypotheses include increased polyol pathway flux, increased formation of advanced glycation end products, activation of protein kinase C, increased flux through the hexosamine pathway, and overproduction of superoxide in mitocbondria. These hypotheses and the links between them are discussed. A new conceptnal framework for future research and drug discovery is prodded.
Keywords:diabetes/complication   diabetic retinopathy/etiology   molecular biology   biochemistry
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