原发性开角型青光眼小梁网细胞氧化损伤的研究进展  

Progress on oxidative stress of trabecular meshwork cells in primary open-angle glaucoma

作　　者：冮晓睿 徐丽娟 韩佳伶 周涛 梁远波 Gang Xiaorui;Xu Lijuan;Han Jialing;Zhou Tao;Liang Yuanbo(The Eye Hospital of Wenzhou Medical University,Glaucoma Research Institute of Wenzhou Medical University,Wenzhou Zhejiang 325027,China)

机构地区：[1]温州医科大学附属眼视光医院,温州医科大学青光眼研究所,浙江温州325027

出　　处：《国际眼科纵览》2024年第6期448-453,共6页International Review of Ophthalmology

基　　金：国家自然科学基金(82201177);浙江省医药卫生项目(2023KY914);国家重点研发计划(2020YFC2008200);浙江省“尖兵”“领雁”研发攻关计划(2022C03112);浙江省万人计划科技创新领军人才(2021R52012);浙江省高校领军人才培养计划(2020099)。

摘　　要：原发性开角型青光眼迄今发病机制不明。近年来,氧化损伤被认为在其发生发展中起重要作用。有学者认为过量的活性氧产生与小梁网功能障碍相关,进而导致房水流出通路病变和随后的眼压升高。但氧化应激和小梁网之间的联系尚未完全了解。本文从氧化应激的来源、小梁网细胞在氧化应激中的分子应答机制及小梁网的功能改变等方面论述原发性开角型青光眼中氧化应激导致小梁网损伤的相关机制。Primary open-angle glaucoma(POAG)is the most common type of glaucoma,while its pathogenesis remains elusive.In recent years,oxidative stress has been recognized as the critical role in POAG formation and progress.Specifically,excessive reactive oxygen species promote the pathogenesis of trabecular meshwork(TM),and lead to the dysfunction of aqueous humor outflow pathway,as well as intraocular pressure elevation.However,the relationship between oxidative stress and TM dysfunction is not fully understood yet.In this article,we aim to elucidate the mechanisms underlying oxidative stress-induced TM damage in POAG,including the oxidative stress sources,the responsive molecular mechanisms of TM cells exposure to oxidative stress,and the structural and functional changes of TM.

关 键 词：原发性开角型青光眼 氧化损伤 小梁网 

分 类 号：R775.2[医药卫生—眼科]