摘要Inhibiting retinal neovascularization is the optimal strategy for the treatment of retina-related diseases,but there is currently no effective treatment for retinal neovascularization.P-element-induced wimpy testis(PIWI)-inte racti ng RNA(piRNA)is a type of small non-coding RNA implicated in a variety of diseases.In this study,we found that the expression of piR-1245 and the interacting protein PIWlL2 were remarkably increased in human retinal endothelial cells cultured in a hypoxic environment,and cell apoptosis,migration,tube formation and proliferation were remarkably enhanced in these cells.Knocking down piR-1245 inhibited the above phenomena.After intervention by a p-JAK2 activator,piR-1245 decreased the expression of hypoxia inducible factor-1α and vascular endothelial growth factor through the JAK2/STAT3 pathway.For in vivo analysis,7-day-old newborn mice were raised in 75±2％hyperoxia for 5 days and then piR-1245 in the retina was knocked down.In these mice,the number of newly formed vessels in the retina was decreased,the expressions of inflammation-related proteins were reduced,the number of apoptotic cells in the retina was decreased,the JAK2/STAT3 pathway was inhibited,and the expressions of hypoxia inducible factor-1α and vascular endothelial growth factor were decreased.Injection of the JAK2 inhibitor JAK2/TYK2-IN-1 into the vitreous cavity inhibited retinal neovascularization in mice and reduced expression of hypoxia inducible factor-1α and vascular endothelial growth factor.These findings suggest that piR-1245 activates the JAK2/STAT3 pathway,regulates the expression of hypoxia inducible factor-1α and vascular endothelial growth factor,and promotes retinal neovascularization.Therefore,piR-1245 may be a new therapeutic target for retinal neovascularization.