缺氧和炎症在视网膜静脉阻塞继发黄斑水肿中的作用

Roles of hypoxia and inflammation in the pathogenesis of macular edema secondary to retinal vein occlusion

视网膜缺氧和炎症因素在视网膜静脉阻塞病变的发展和转归中扮演重要角色。视网膜缺氧导致低氧诱导因子-1α(HIF-1α)表达上调,促进下游血管内皮生长因子(VEGF)、胎盘生长因子(PLGF)及其受体表达增加;炎性细胞主要包括视网膜内源的小胶质细胞以及来自血液中趋化与浸润的白细胞,尤以单核-巨噬细胞活化为主;炎性因子包括白介素IL-1β、IL-6、IL-8、肿瘤坏死因子-α(TNF-α)及单核细胞趋化因子-1(MCP-1)等大量生成和增加;炎性介质主要是由崩解的血细胞产生,细胞膜脂质在磷脂酶A2、脂氧酶和环氧酶的作用下,产生大量的炎性介质如白三烯及前列腺素类等。在视网膜缺氧和炎性因素共同作用下,视网膜多种病理性改变包括血-视网膜屏障破坏、视网膜血管渗漏增加、黄斑水肿加剧,视网膜无灌注区形成及扩大,视网膜新生血管形成及视网膜内层萎缩变薄等。因此早期抗VEGF和抗炎对治疗视网膜静脉阻塞继发黄斑水肿至关重要。(国际眼科纵览,2022,46:173-178)

Retinal hypoxia and inflammation play important roles in the progression and outcome in retinal vein occlusion(RVO).Retinal hypoxia leads to the up-regulation of hypoxia-inducible factor-1α(HIF-1α),which promotes the expression of its downstream targets,such as VEGF,PLGF and the receptors,etc.Inflammatory cells mainly include retinal endogenous microglia and the exogenous leukocytes,especially the activated monocyte-macrophage,which are chemotactic and infiltrate in retina from the blood.Inflammatory factors including IL-1β,IL-6,IL-8,TNF-αand MCP-1 are produced and released in large quantities,and the inflammatory mediators are mainly produced from the disintegrated blood cells.A large number of inflammatory mediators,such as leukotrienes and prostaglandins,were produced from the cell membrane lipids under the action of phospholipase A2,lipoxygenase and cyclooxygenase.Under the combined action of retinal hypoxia and inflammation,a variety of pathological changes were observed in retina,such as the breakdown of the blood-retinal barrier,increased retinal vascular leakage,and macular edema,the appearance and expansion of non-perfusion areas,retinal neovascularization,the atrophy and thinness of inner retina,and so on.Therefore,early treatments with anti-VEGF and anti-inflammation therapies are of great importance for the treatment of macular edema secondary to RVO.(Int Rev Ophthalmol,2022,46:173-178)