Cui Na, Jia Jun, He Yuan
Department of Ophthalmology, the Second Affiliated Hospital of Xi'an Medical University, Xi'an 710038, Shaanxi Province, China.
Xi'an Key Laboratory for the Prevention and Treatment of Eye and Brain Neurological Related Diseases, Xi'an 710038, Shaanxi Province, China.
Int J Ophthalmol. 2025 Jan 18;18(1):160-167. doi: 10.18240/ijo.2025.01.20. eCollection 2025.
Glaucoma is a group of diseases characterized by progressive optic nerve degeneration, with the characteristic pathological change being death of retinal ganglion cells (RGCs), which ultimately causes visual field loss and irreversible blindness. Elevated intraocular pressure (IOP) remains the most important risk factor for glaucoma, but the exact mechanism responsible for the death of RGCs is currently unknown. Neurotrophic factor deficiency, impaired mitochondrial structure and function, disrupted axonal transport, disturbed Ca homeostasis, and activation of apoptotic and autophagic pathways play important roles in RGC death in glaucoma. This review was conducted using Web of Science, PubMed, Project, and other databases to summarize the relevant mechanisms of death of RGCs in glaucoma, in addition to outlining protective treatments to improve the degradation of RGCs.
青光眼是一组以进行性视神经变性为特征的疾病,其特征性病理变化是视网膜神经节细胞(RGCs)死亡,最终导致视野缺损和不可逆性失明。眼压升高仍然是青光眼最重要的危险因素,但RGCs死亡的确切机制目前尚不清楚。神经营养因子缺乏、线粒体结构和功能受损、轴突运输中断、钙稳态紊乱以及凋亡和自噬途径的激活在青光眼RGCs死亡中起重要作用。本综述利用科学网、PubMed、科研项目及其他数据库进行,旨在总结青光眼RGCs死亡的相关机制,此外还概述了改善RGCs退变的保护性治疗方法。