Mounting evidence suggests that immunological mechanisms play a fundamental role in the pathogenesis of diabetic retinopathy (DR) and diabetic macular edema (DME). Upregulation of cytokines and other proinflammatory mediators leading to persistent low-grade inflammation is believed to actively contribute to the DR-associated damage to the retinal vasculature, inducing breakdown of the blood-retinal barrier, subsequent macular edema formation, and promotion of retinal neovascularization. This review summarizes the current knowledge of the biological processes providing an inflammatory basis for DR and DME. In addition, emerging therapeutic approaches targeting inflammation are discussed, including blockade of angiopoietin 2 and other molecular targets such as interleukin (IL)-6, IL-1β, plasma kallikrein, and integrins.

中文翻译：

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炎症在糖尿病眼病中的作用。

越来越多的证据表明，免疫机制在糖尿病性视网膜病变（DR）和糖尿病性黄斑水肿（DME）的发病机理中起着基本作用。据信导致持续的低度炎症的细胞因子和其他促炎介质的上调积极地导致与DR相关的视网膜脉管系统损伤，引起血视网膜屏障的破坏，随后的黄斑水肿形成以及视网膜新血管形成的促进。这篇综述总结了生物过程的当前知识，为DR和DME提供了炎性基础。另外，讨论了针对炎症的新兴治疗方法，包括阻断血管生成素2和其他分子靶标，例如白介素（IL）-6，IL-1β，血浆激肽释放酶和整联蛋白。