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青光眼视网膜神经节细胞凋亡途径:起始机制和下游机制

Retinal ganglion cell apoptotic pathway in glaucoma: Initiating and downstream mechanisms.

作者信息

Levkovitch-Verbin Hani

机构信息

Glaucoma Service, Goldschleger Eye Institute, Sheba Medical Center, Tel-Hashomer, Israel; Sackler Faculty of Medicine, Tel-Aviv University, Tel-Hashomer, Israel.

出版信息

Prog Brain Res. 2015;220:37-57. doi: 10.1016/bs.pbr.2015.05.005. Epub 2015 Oct 1.

Abstract

Apoptosis of retinal ganglion cells (RGCs) in glaucoma causes progressive visual field loss, making it the primary cause of irreversible blindness worldwide. Elevated intraocular pressure and aging, the main risk factors for glaucoma, accelerate RGC apoptosis. Numerous pathways and mechanisms were found to be involved in RGC death in glaucoma. Neurotrophic factors deprivation is an early event. Oxidative stress, mitochondrial dysfunction, inflammation, glial cell dysfunction, and activation of apoptotic pathways and prosurvival pathways play a significant role in RGC death in glaucoma. The most important among the involved pathways are the MAP-kinase pathway, PI-3 kinase/Akt pathway, Bcl-2 family, caspase family, and IAP family.

摘要

青光眼患者视网膜神经节细胞(RGCs)的凋亡会导致进行性视野缺损,使其成为全球不可逆性失明的主要原因。青光眼的主要危险因素——眼压升高和衰老,会加速RGCs的凋亡。人们发现,青光眼患者RGCs死亡涉及众多途径和机制。神经营养因子剥夺是早期事件。氧化应激、线粒体功能障碍、炎症、胶质细胞功能障碍以及凋亡途径和促生存途径的激活在青光眼患者RGCs死亡中起重要作用。其中最重要的途径包括丝裂原活化蛋白激酶(MAP)途径、磷脂酰肌醇-3激酶(PI-3激酶)/蛋白激酶B(Akt)途径、Bcl-2家族、半胱天冬酶家族和凋亡抑制蛋白(IAP)家族。

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