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.(国际眼科纵览,2024,48:448-453)
Abstract
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 PO-AG formation and progress.Specifically,excessive reactive oxygen species promote the pathogenesis of tra-becular meshwork(TM),and lead to the dysfunction of aqueous humor outflow pathway,as well as intraoc-ular 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.(Int Rev Ophthalmol,2024,48:448-453)
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