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糖尿病患者血视网膜屏障的改变:细胞因子和活性氧。

Alterations to the blood-retinal barrier in diabetes: cytokines and reactive oxygen species.

机构信息

Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, Pennsylvania, USA.

出版信息

Antioxid Redox Signal. 2011 Sep 1;15(5):1271-84. doi: 10.1089/ars.2011.3906. Epub 2011 May 11.

Abstract

Diabetic retinopathy (DR) is a leading cause of blindness in Western society. Since the prevalence of diabetes continues to increase dramatically, the impact of DR will only worsen unless new therapeutic options are developed. Recent data demonstrate that oxidative stress contributes to the pathology of DR and inhibition of oxidative stress reduces retinal vascular permeability. However, direct mechanisms by which oxidative stress alters the blood-retinal barrier (BRB) and increases vascular permeability remain to be elucidated. A large body of evidence demonstrates a clear role for altered expression of cytokines and growth factors in DR, resulting in increased vascular permeability, and the molecular mechanisms for these processes are beginning to emerge. The pathology of DR is likely a result of metabolic dysregulation contributing to both oxidative stress and cytokine production. This review will examine the evidence for oxidative stress, growth factors, and other cytokines in tight junction regulation and vascular permeability in DR.

摘要

糖尿病性视网膜病变(DR)是西方社会致盲的主要原因。由于糖尿病的患病率继续急剧增加,除非开发出新的治疗选择,否则 DR 的影响只会恶化。最近的数据表明,氧化应激导致 DR 的病理学发生,抑制氧化应激可降低视网膜血管通透性。然而,氧化应激改变血视网膜屏障(BRB)并增加血管通透性的确切机制仍有待阐明。大量证据表明,细胞因子和生长因子的表达改变在 DR 中起着明显的作用,导致血管通透性增加,这些过程的分子机制开始出现。DR 的病理学可能是代谢失调的结果,导致氧化应激和细胞因子的产生。本综述将探讨 DR 中紧密连接调节和血管通透性中氧化应激、生长因子和其他细胞因子的证据。

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