小梁网异常与原发性开角型青光眼的关系  

Relationship between trabecular meshwork abnormalities and primary open angle glaucoma

作　　者：叶俏娜 余敏斌[1] 杨扬帆[1] Ye Qiaona;Yu Minbin;Yang Yangfan(State Key Laboratory of Ophthalmology,Zhongshan Eye Center,Sun Yatsen University,Guangzhou 510060,China)

机构地区：[1]中山大学中山眼科中心眼科学国家重点实验室,广州510060

出　　处：《国际眼科纵览》2022年第2期150-156,共7页International Review of Ophthalmology

基　　金：广东省自然科学基金(2021A1515010604)。

摘　　要：原发性开角型青光眼中小梁网细胞结构和功能发生异常,房水外排阻力增大从而形成病理性高眼压。小梁网细胞在转化生长因子β(TGF-β)介导的Rho-GTPase途径作用下,细胞骨架改变,形成交联肌动蛋白网络,在TGF-β介导经典Smad核传导通路以及非经典Smad途径作用下,细胞外基质堆积,形成交联化。通过细胞-基质相互作用,造成小梁网硬度增大,顺应性减弱。线粒体和溶酶体长期受到外源性和内源性诱导的活性氧自由基(ROS)攻击,细胞老化加剧,水解组织蛋白酶释放,自噬通量下降,细胞凋亡激活。本综述探讨小梁网细胞、微环境及其相互影响机制,为进一步探究原发性开角型青光眼发病机制提供参考。(国际眼科纵览,2022,46:150-156)The structural and functional abnormalities of trabecular meshwork increase resistance to drainage of aqueous humor in primary open-angle glaucoma(POAG),resulting in pathologically high intraocular pressure.Trabecular meshwork reshape the cytoskeleton and form cross-linked act in network under transforming growth factor(TGF)-β-mediated Rho-GTPase pathway.Extracellular matrix accumulates and forms crosslinking through TGF-β-mediated Smad nuclear pathway and non-classical Smad pathway.Cell-matrix interaction increases the hardness and decreases the compliance of the trabecular meshwork.Cell aging and autophagy dysfunction activate apoptosis through exogenously and endogenously reactive oxygen species(ROS)attack.This review will discuss the interaction between trabecular meshwork and the microenvironment,providing further information to explore pathogenesis of POAG.(Int Rev Ophthalmol,2022,46:150-16)

关 键 词：原发性开角型青光眼 小梁网细胞骨架 细胞外基质 

分 类 号：R775.2[医药卫生—眼科]