Proliferative vitreoretinopathy(PVR)is a serious complication that occurs in the natural history of rhegmatogenous retinal detachment(RRD)or after retinal detachment surgery, often resulting in vision loss. Currently, there has no effective treatment. The pathological characteristics of PVR are the excessive inflammatory response and abnormal proliferation of various cells under the action of cytokines, which eventually form a layer of proliferative membrane around the retinal surface, and further lead to traction retinal detachment(TRD). In-depth studies on the pathogenesis of PVR will help to find promising molecular targets for its treatment. Recent studies have found that vascular endothelial growth factor(VEGF)and the epithelial-mesenchymal transition(EMT)of retinal pigment epithelium(RPE)cells play an important role in the pathogenesis of PVR. This article summarizes the roles of VEGF and RPE cell EMT in the pathogenesis of PVR and the interaction mechanism between them, with the aim to provide new ideas for the treatment and clinical research of PVR.