青光眼视神经损害机制  

Mechanisms of glaucomatous optic neuropathy

作　　者：王余萍[1] 袁源智[1] 

机构地区：[1]复旦大学附属中山医院眼科复旦大学循证医学中心,上海200032

出　　处：《中国临床医学》2016年第5期667-671,共5页Chinese Journal of Clinical Medicine

基　　金：上海市自然科学基金(11DZ1921206)~~

摘　　要：青光眼是一组以视神经萎缩和视野缺损为共同特征的进行性的视神经退行性疾病。视网膜神经节细胞(retinal ganglion cell,RGC)的渐进性死亡和轴突的丢失是青光眼的重要特征,严重时导致患者不可逆视力丧失。目前认为,青光眼视神经损害(glaucomatous optic neuropathy,GON)可由多种因素引起,除了机械学说和缺血学说,还有神经因素、氧化应激作用、免疫因素等多种因素的参与,遗传和生活方式也可能影响其发生发展。GON的发病机制尚未阐明。本文就近年来GON机制的研究作一综述,以期为视神经损害的预防及治疗提供参考依据。Glaucoma is a group of progressive optic neurodegenerative diseases with common features of optic atrophy and visual field defects.Progressive death of retinal ganglion cells and loss of axons are important features of glaucoma,which eventually lead to irreversible visual loss in severe cases.At present,glaucomatous optic neuropathy（GON）can be caused by many factors--apart from the mechanical theory and vascular ischemia theory,the two most prevalent hypotheses on the pathomechanisms of GON,neural factors,oxidative stress and immune factors are also involved.Genetic factors and lifestyle may also affect its occurrence and development.The mechanism of GON has not been fully understood.This article reviews the recent studies on the mechanism of GON,and hopefully provides new insights into the prevention and treatment of optic nerve damage.

关 键 词：青光眼 视神经病变 机制 

分 类 号：R775.2[医药卫生—眼科]