长链非编码RNA MALAT1对缺血性视网膜病变新生血管形成的调控作用研究进展  

Research progress on the regulatory effect of lncRNA MALAT1 on neovascularization in ischemic retinopathy

作　　者：李兆金(综述) 底煜(审校)[1] Li Zhaojin;Di Yu(Department of Ophthalmology,Shengjing Hospital of China Medical University,Shenyang 110000,China)

机构地区：[1]中国医科大学附属盛京医院眼科,沈阳110000

出　　处：《中华实验眼科杂志》2025年第1期92-96,共5页Chinese Journal Of Experimental Ophthalmology

摘　　要：缺血性视网膜病变(IRs)伴新生血管形成常严重损伤视力甚至导致失明。研究表明,长链非编码RNA(LncRNA)MALAT1与调控视网膜细胞发育过程中的蛋白编码基因共表达。近年来的研究也证实了MALAT1在IRs中表达上调,具有诱导氧化应激和炎症反应,促进血管内皮细胞增殖、迁移及血管生成,改变表观遗传修饰等作用,在视网膜新生血管形成的发病机制和调控中起着重要作用。本文从IRs的发病机制,MALAT1在视网膜中的表达和功能及其在血管生成、氧化应激、炎症、血管内皮损伤、表观遗传调控、细胞周期等方面的作用总结MALAT1在IRs中的研究现状,探讨其在视网膜新生血管形成发生和发展中的作用,更深入地了解MALAT1在IRs新生血管形成中的作用机制将有助于开发其靶向治疗策略。Ischemic retinopathies(IRs)with neovascularization often severely impair vision and even lead to blindness.Studies have shown that long non-coding RNA(lncRNA)MALAT1 is co-expressed with protein-coding genes that regulate retinal cell development.Recent studies have also confirmed that MALAT1 is up-regulated in IRs and has the effects of inducing oxidative stress and inflammatory responses,promoting vascular endothelial cell proliferation,migration and angiogenesis,and changing epigenetic modifications,which plays an important role in the pathogenesis and regulation of retinal neovascularization.This article summarizes the current research status of MALAT1 in IRs from the aspects of the pathogenesis of IRs,the expression and function of MALAT1 in the retina and its role in angiogenesis,oxidative stress,inflammation,vascular endothelial damage,epigenetic regulation,cell cycle,etc.,and explores its role in the occurrence and development of retinal neovascularization to provide a deeper understanding of the mechanism of MALAT1 in the neovascularization of IRs to help develop its targeted treatment strategies.

关 键 词：长链非编码RNA 表观遗传 氧化应激 肺腺癌转移相关转录本1 缺血性视网膜病变 

分 类 号：R774.1[医药卫生—眼科]