视网膜神经节细胞（RGCs）凋亡是青光眼视觉损害的病理基础，研究表明缺血再灌注损伤是急性闭角型青光眼RGCs凋亡的主要原因。前期研究发现急性高眼压导致视网膜miRNAs表达改变，部分差异表达miRNAs可能参与RGCs凋亡调控。近期我们在体外缺血再灌注RGCs凋亡模型中发现RGCs内miR-350表达上升，靶基因XIAP表达下降，活化Caspase-3水平增加。据此推断：缺血再灌注损伤导致miR-350表达上升、抑制靶基因XIAP表达，Caspases凋亡信号通路继而被激活，从而促进RGCs凋亡。为验证此假说，本研究拟体内、体外干预miR-350表达，探究miR-350对XIAP/Caspases信号轴的调控，多层面分析其对RGCs凋亡的影响，以期阐明miR-350调控RGCs凋亡分子机制。该研究有望从miRNAs角度阐释RGCs凋亡调控机制，为青光眼视神经保护治疗提供新思路。

Apoptosis of retinal ganglion cells (RGCs) is the important pathologic basis of visual impairment in glaucoma. Numerous studies have shown that ischemia-reperfusion injury is the main reason for RGCs apoptosis in acute angel-closure glaucoma. Our previous results have showed that acute ocular hypertension led to changes in the expression of miRNAs, whose target genes were associated with the regulation of RGCs apoptosis. Recently, we found that vitro ischemia-reperfusion injury induced significant upregulation of miR-350 in RGCs, down-regulation of target gene- X-linked Inhibitor of Apoptosis Protein (XIAP) and activated Caspase-3 increased subsequently. Therefore, we assumed that miR-350 increased under ischemia-reperfusion injury, XIAP was inhibited and Caspases were activated subsequently, RGCs apoptosis was induced therefore. To verify our hypothesis, vivo and vitro ischemia-reperfusion injury were used to evaluate RGCs apoptosis due to the change of miR-350 expression. The regulation of miR-350 on XIAP/Caspases signaling axis and RGCs apoptosis were explored. The expected result of this study is to illustrate the mechanism of miRNAs regulation on RGCs apoptosis, which might offer a novel perspective of RGCs apoptosis and provide novel idea for the development of neuroprotective drugs for glaucoma.