糖尿病性视网膜病变（DR）是主要的致盲性眼病，视网膜微血管病变是其致病根本，但机制尚未完全阐明。越来越多的研究证明环状RNA与疾病的发生发展密切相关，然而，环状RNA在DR微血管病变中的作用还亟待研究。我们初步研究发现，circZW10在增殖期DR患者纤维血管膜和高糖诱导的人视网膜微血管内皮细胞损伤模型中表达降低，过表达circZW10显著减轻高糖诱导的视网膜微血管内皮细胞损伤，circZW10与miR-31-5p存在相互作用。因此，我们推测circZW10通过吸附miR-31-5p，减少其对下游靶基因LATS2的抑制，从而参与DR微血管病变。本课题拟在增殖期DR患者临床标本、糖尿病大鼠模型和高糖损伤细胞模型上，利用多种生物学技术，深入研究circZW10对DR微血管病变的调控作用，揭示circZW10/miR-31-5p/LATS2网络的作用机制。研究成果有望为DR的早期防治提供新策略。

Diabetic retinopathy (DR) is one of the leading causes of blindness. Retinal microvascular dysfunction is the primary factor of visual loss in DR. However, the underlying mechanism is not yet well understood. Growing evidence suggests that circular RNAs (circRNA) are involved in the occurrence and development of various diseases. However, the role of circRNA in diabetic retinal microvascular dysfunction remains unclear. Our preliminary study indicated that the level of circZW10 was downregulated in the retinal proliferative fibrovascular membranes of patients with DR and high glucose (HG)-treated human retinal microvascular endothelial cells (HRMEC). circZW10 overexpression significantly alleviated the HRMEC injury induced by HG treatment. Further study suggested that circZW10 acted as a sponge of miR-31-5p. Therefore, we hypothesized that circZW10 sponged miR-31-5p and relieved the inhibitory effect of miR-31-5p on LATS2, a downstream regulator, to regulate retinal microvascular dysfunction under diabetic conditions. In this study, we aim to investigate the role of circZW10 and the regulatory mechanism of circZW10/miR-31-5p/LATS2 network in diabetic retinal microvascular dysfunction in clinical specimens, diabetic rat model and HG-treated HRMECs through applying multiple biological techniques. The purpose of the study is to provide a novel strategy for the prevention and early treatment of DR.