早产儿视网膜病变(ROP)是发生在早产儿的一种血管增生性的玻璃体视网膜疾病,其主要病理性改变是视网膜血管闭塞、缺血缺氧诱发病理性新生血管形成,进而导致视网膜脱离,甚至失明.这类增生性血管病变涉及多条信号通路,对于分子机制的深入理解更有利于靶向治疗病理性新生血管.就ROP发病机制中的有关信号通路进行综述,主要包括Wnt-信号通路成员在病理性血管发展中的作用,CCN1蛋白与富含半胱氨酸蛋白61(CCN1/Cry61)在提高视网膜血管的生理性适应和减少病理性新生血管生成方面的重要作用,Janus激酶/信号转导子与转录激活子(JAK/STAT)信号通路诱导视网膜和玻璃体内新生血管的形成,Apelin蛋白与血管紧张素1型受体相关蛋白(Apelin/A PJ)信号通路对于视网膜血管发生、血管塑形的影响以及在低氧条件下引发新生血管形成.“,”Retinopathy of prematurity (ROP) is a kind of vasoproliferative disorders,which leads to vision loss even blindness in premature neonates.Major pathogenesis in ROP is vascular occlusion and retinal neovascularization precipitated by ischemia and hypoxia.Proliferative retinopathy is asscioated with several signaling pathways,such as Wnt signaling pathway,CCN1/cysteine-rich 61 (CCN1/Cry61) in pathological neovascularization,JAK/STAT (Janus kinase/signal transducer and activator of transcription) in intravitreous neovascularization,Apelin/ APJ (Apelin/angiotensin type Ⅰ receptor related protein) in pathological retinal angiogenesis.Deep understanding of the pathways is conducive to treat proliferative retinopathy by targeting pathologic neovessels.