Abstract: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.
