视神经损伤以神经节细胞(RGCs)的损伤死亡为核心病理环节，最终导致不可逆视功能损害。自噬作为一种可调节的细胞降解和死亡机制，广泛参与肿瘤、神经损伤、自身免疫疾病等多种疾病病理过程。现有研究表明，视神经损伤后，自噬水平显著上调并呈现双重特性，即在早期可能介导细胞损伤，而在随后的阶段则更多地表现为神经保护和轴突再生。此外，小胶质细胞的自噬激活可能在调控其活化表型和神经炎症中发挥重要作用。如何精准调控自噬促进RGCs存活和改善视功能，成为治疗视神经损伤的关键研究方向。文章综述了自噬在视神经损伤中的作用及其研究进展。

The damage and death of retinal ganglion cells(RGCs)are central pathological events in optic nerve injury, leading to irreversible visual impairment. Autophagy, a regulated process of cellular degradation and death, is involved in the pathogenesis of various diseases, including tumors, neurological damage, and autoimmune disorders. Current research indicates that autophagy is significantly upregulated following optic nerve injury, exhibiting a dual role: while it may mediate cellular damage in the early stages, it tends to promote neuroprotection and axonal regeneration in later phases. Moreover, the activation of autophagy in microglia may play a crucial role in regulating their activation phenotype and neuroinflammation. Precisely modulating autophagy to promote RGCs survival and improve visual function has become a key challenge in the treatment of optic nerve injury. This review summarizes the role of autophagy in optic nerve injury and its therapeutic interventions.

国家自然科学基金资助项目(No. 82101112,82471082)