长期高血糖是发生糖尿病视网膜病变(DR)的决定因素，血液中的葡萄糖依靠葡萄糖转运蛋白1(GLUT1)进入视网膜。课题组前期已报道抑制视网膜GLUT1表达可有效缓解DR，但其上游调控机制尚不明确。我们利用生物信息学分析构建了circ_0036564─miR-620─GLUT1 ceRNA调控网络并进行初步验证，提示该ceRNA调控网络参与了DR发病。基于研究背景和前期工作基础，课题组提出科学假设：糖尿病条件下circ_0036564表达上调，作为ceRNA竞争性与miR-620结合而降低miR-620表达丰度，解除miR-620对GLUT1 mRNA的抑制，从而上调GLUT1表达，促进DR。本项目拟从细胞和动物两个水平研究并证实1.circ_0036564─miR-620─GLUT1存在ceRNA机制;2.circ_0036564可通过调控GLUT1而促进DR发病，为DR治疗提供新思路。

Long-term hyperglycemia is the key factor of the development of diabetic retinopathy (DR). Glucose transporter 1 (GLUT1) facilitate glucose enter the retina from blood. Our previous study found that suppression of GLUT1, limiting the glucose concentration of the retina, could effectively alleviate DR,but its upstream regulation remains unknown. We also used bioinformatics analysis to construct circ_0036564-miR-620-GLUT1 regulatory network and preliminarily verified that the ceRNA regulatory network was involved in the pathogenesis of DR. Based on research background and previous data , we proposed the scientific hypothesis: circ_0036564 expression was upregulated in diabetes condition, and competed with miR-620 as a ceRNA, releasing the inhibition of miR-620 against GLUT1 expression, thus involved in the progression of DR. This project aims to investigate: 1.the relationship of ceRNA regulation between circ_0036564-mir-620-GLUT1. 2.circ_0036564 can promote the pathogenesis of DR by regulating GLUT1 and provide new ideas for the treatment of DR.