青光眼是一组以视网膜神经节细胞(RGCs)渐进性死亡及其轴突慢性退化为特征的神经退行性疾病，主要与病理性眼压升高有关。自噬，即细胞自我“消化”，是一种细胞降解、回收机制。过度自噬或自噬受损均可能导致细胞功能障碍，甚至死亡。近年的研究表明，自噬与不同因素导致的青光眼小梁网细胞功能异常和RGCs凋亡及视神经退行性改变密切相关，其中主要包括氧化应激、机械性刺激、眼压升高、轴突损伤、遗传因素等。调控自噬保护RGCs可能为青光眼的治疗提供新的方法。本文就自噬的定义及分类、自噬的调控、自噬在氧化应激及机械性刺激过程中对小梁网细胞的作用、自噬在高眼压环境下及RGCs轴突损伤后对RGCs的作用和自噬在RGCs中与凋亡的关系、自噬与遗传性视神经变性、基因及药物调控自噬治疗青光眼的最新研究结果进行综述。“,”Glaucoma, a neurodegenerative disease characterized by progressive death of retinal ganglion cells (RGCs) and chronic axonal degeneration, is often associated with elevated intraocular pressure.Autophagy, which means self-eating, is a mechanism of cell degradation and recycling.Excessive autophagy or impaired autophagy may lead to cell dysfunction and even cell death.Recent studies have shown that autophagy is closely related to trabecular meshwork cell dysfunction, RGCs apoptosis and optic nerve degeneration caused by different factors, including oxidative stress, mechanical stimulation, high intraocular pressure, axon injury, genetic factors and so on.Regulating autophagy to protect RGCs may provide new ideas for glaucoma treatments.In this article, the definition and classification of autophagy, the regulation of autophagy, the role of autophagy in the process of oxidative stress and mechanical stimulation on the function of trabecular meshwork cells, and the impact of autophagy on RGCs under high intraocular pressure and RGCs axonal injury, the relationship between autophagy and apoptosis in RGCs, as well as the latest research results on autophagy and hereditary optic nerve degeneration, regulation of autophagy via gene and drug for the treatment of glaucoma were reviewed.