外伤性视神经病变是因外力损伤视神经，进而严重损害视力的致盲性眼病。自噬是一种细胞内降解途径，有助于维持细胞正常组分合成与受损细胞器及有毒细胞成分的分解之间的平衡。视神经受创后，视神经和视网膜中自噬标志物增加。自噬在外伤性视神经病变的不同阶段对视网膜神经节细胞可能起不同作用。多数研究表明，上调自噬可以减轻外伤性视神经病变中视网膜神经节细胞的死亡；也有研究提示在视神经损伤后极早的时期抑制自噬可以抑制视网膜神经节细胞轴突变性。该文对自噬的定义及功能、自噬的发生机制、视神经创伤后自噬水平改变、自噬在视神经创伤后对视网膜神经节细胞的作用的研究结果进行综述。

Traumatic optic neuropathy is a blinding eye disease that causes severe damage to vision due to external force damage to the optic nerve.. Autophagy is an intracellular degradation pathway that helps maintain the balance between the synthesis

of normal cell components and the breakdown of damaged organelles and toxic cellular components. Autophagy markers are increased in optic nerve and retina after optic nerve trauma. Autophagy may play different roles on retinal ganglion cells (RGCs) at different stages of traumatic optic neuropathy. Most studies have shown that upregulating autophagy can attenuate RGCs death in traumatic optic neuropathy; however, it has also been suggested that inhibition of autophagy at ultra-early stage after injury can inhibit RGCs axonal degeneration. In this review, we reviewed the definition and function of autophagy, the mechanism of autophagy, and summarized the change of autophagy level after optic nerve trauma, as well as the effects of autophagy in RGCs after optic nerve trauma.