新生血管是早产儿视网膜病变（Retinopathy of prematurity, ROP）的重要病理改变之一。Wnt信号通路参与ROP新生血管的发生发展，但其表观遗传调控机制未明。环状RNA（circRNA）可通过吸附微小RNA（miRNA）来调节靶基因的表达。我们对ROP模型鼠进行基因转录组生物芯片检测和生物信息数据分析，发现新生血管发生时circRNA_2984、Wnt7a表达升高，miR-1894-3p表达下调；miR-1894-3p具有与circ_2984,Wnt7a特异结合的序列。我们推测，环境因素诱导circ_2984升高后可能通过吸附游离的miR-1894-3p，导致下游靶基因Wnt7a表达上调，诱发新生血管的产生。本项目拟从分子、细胞和整体水平，开展体内和体外的功能实验，探讨circ_2984-miR-1894-3p-Wnt7a轴调节ROP模型鼠新生血管的致病机制。

Neovascularization is the crucial pathological process underlying retinopathy of prematurity (ROP), in which Wnt signaling pathway is involved. However, the epigenetic regulation of Wnt pathway in ROP requires to be further elucidated. Circular RNA (circRNA), a novel class of molecule of competing endogenous RNAs, can regulate gene expression by sponging microRNA (miRNA). Based on our current transcriptome chip (mRNA, circRNA, miRNA) data and bioinformatics analysis, we revealed an elevated level of circRNA_2984 and Wnt7a，and a reduced level of miR-1894-3p simultaneously in ROP mouse model. Moreover, miR-1894-3p contains miRNA response elements that could potentially interact with cirRNA_2984 and Wnt7a. Thus, we hypothesized a circ_2984-miR1894-3p-Wnt7a axis regulating the process of neovascularization. We hereby intend to determine the functional role of circ_2984-miR1894-3p-Wnt7a axis in ROP neovascularization via combination of in vitro (biochemistry and cell biology methods) and in vivo (mouse models) experiments. This study aims to unveil a novel regulatory mechanism of ROP neovascularization in perspective of competing endogenous RNA network and sheds new light on future clinical therapies development for ROP.