免疫炎症诱导的RGCs损害是急性青光眼，视网膜血管性疾病等缺血再灌注损伤相关疾病视功能损害的重要原因。调控视网膜小胶质细胞由M1表型向M2表型极化是抑制免疫炎症保护RGCs可行方法。我们在LPS诱导的眼内炎症中发现Notch1信号通路调控M1/M2极化，对视网膜缺血再灌注损伤的研究也提示Notch1是小胶质细胞极化和炎症调控的可能靶点。新近研究发现自噬在脑部小胶质细胞极化调控中发挥重要作用。已有研究发现Notch1信号通路的活化受到自噬的调控。由此，我们提出假设，在视网膜缺血再灌注损伤中自噬可能通过Notch1信号通路调控小胶质细胞极化，从而达到减轻炎症和保护RGCs的作用。我们拟通过体外实验探讨自噬在视网膜小胶质细胞极化调控中的作用和机制，在视网膜缺血再灌注损伤动物模型中观察其在炎症调控和RGCs保护中的作用，为临床缺血再灌注相关疾病的视功能保护治疗寻找新的思路和理论支持。

Inflammation-induced RGCs injury is the common cause of visual impairment in acute glaucoma, retinal vascular diseases and other diseases related to retinal ischemia reperfusion injury(I/R). Regulating retinal microglia cells from pro-inflammatory M1 phenotype to anti-inflammatory M2 phenotype can reduce inflammation and protect RGCs. Our previous studies showed that Notch1 signaling pathway plays an important role in the regulation of LPS-induced microglia polarization，and Notch1 is a potential target for microglial polarization and inflammatory regulation in retinal ischemia reperfusion injury. Recent studies have found that autophagy is involved in the regulation of microglial cell polarization in central nervous system, but not reported in retina. Autophagy can regulate the activation of Notch1 signaling pathway. Therefore, we proposed a reasonable hypothesis that autophagy may regulate the polarization of retinal microglia cells through Notch1 signaling pathway, through which the inflammation is inhibited and RGCs survival is promoted in ischemia-reperfusion injury. Current study intends to explore the role and mechanism of autophagy on microglia polarization, inflammation regulation and RGCs protection in vitro and in vivo, to provide a new therapeutic strategy for the I/R injury related diseases.