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青光眼是以视网膜神经节细胞(RGCs)进行性丧失、视盘生理性凹陷扩大、视野缺失为特征的进行性视神经退行性疾病,其神经损伤的确切病变尚未明确.自噬是人体内一条重要的代谢途径,它在降解和循环利用受损细胞器,细胞内大分子物质在维持细胞内稳态方面具有重要作用,并参与多种疾病的发生和发展.近年来对自噬与青光眼的关系研究提示我们,自噬在青光眼视神经病变的转归过程中发挥双刃剑作用,体内有多条代谢通路对自噬过程进行调控,深入理解并利用自噬作用对青光眼视神经病变进行治疗研究具有重要意义.本文就自噬在高眼压、视神经纤维层损伤、视盘重塑、异常蛋白清除以及免疫反应等青光眼视神经病变的发病及其调控机制方面的相关研究进展进行综述.“,”Glaucoma is a chronic neurodegenerative disease of optic nerve accompanied by apoptosis of retinal ganglion cells (RGCs),cupping of optic nerve head,and visual field loss.The mechanism of glaucomatous optic neuropathy still has not yet been elucidated.Autophagy is an important metabolic pathway including degrading and recycling damaged organelles and macromolecules to maintain intracellular homeostasis,and it participates in the pathogenesis of various diseases.Some studies on the relationship between autophagy and glaucoma indicated that autophagy played a dual role during the glaucomatous neurodegenerative process,and it is verified that many metabolic pathways modulate autophagy by positive and negative regulation.To elucidate and take advantage of autophagy to manage neurodegeneration in glaucoma is of great importance.In this article,the probable effects of autophagy in the mechanism of glaucomatous optic neuropathy including ocular hypertension,damage to the optic nerve fiber layer,remodeling of optic nerve head,clearance of mutant protein,and immune reactions are reviewed.