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机构地区:[1]复旦大学附属上海市第五人民医院眼科,上海200240
出 处:《眼科研究》2007年第9期710-713,共4页Chinese Ophthalmic Research
摘 要:糖尿病视网膜病变(DR)是严重的糖尿病眼部并发症之一。研究表明,氧化应激和应激激活的信号通路与DR有着密切关系。高糖通过多种机制刺激活性氧类物质的产生,从而生长因子和细胞因子的基因表达。正常情况下,过多的活性氧物质可被抗氧化防御系统清除,但持续性高血糖情况下过多的活性氧物质可导致细胞损害,包括视网膜内皮细胞、周细胞和视网膜节细胞。现就氧化应激在DR发生发展中所起的作用做一综述。Chronic hyperglycemia is a major initiator of diabetic vascular complications. Diabetic retinopathy is the most severe situation of the several ocular complications of diabetes and still a leading cause of blindness. High glucose, via various mechanisms such as increase of production of advanced glycation end products, activation of protein kinase C, stimulation of the polyol pathway and enhance of reactive oxygen species (ROS) generation, altered gene expression of growth factors and cytokines. Recent studies show that hyperglycemia-induced mitochondrial superoxide production plays a major role in the development and progression of diabetic retinopathy. Normally, over production of ROS resulting in oxidative stress could be completely cleared by antioxidative defense system. However,excessive ROS from oxidative stress under persistent hyperglycemia could lead to the damage of cells including retinal endothelial cells, pericytes and ganglion cells. This review focus on the relationship between oxidative stress and diabetic retinopathy.
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