晶状体上皮细胞（LECs）中的氧化应激反应和自噬活动失调参与了白内障的发病过程。课题组前期研究发现：糖尿病性白内障LECs中miR-30a-5p表达下降，可负性调控靶基因TP53INP1增强氧化应激反应，也可负性调控靶基因BECN1增强自噬活动；在持续性高糖状态下，LECs的氧化应激和自噬呈现动态变化并相互影响。为进一步了解miR-30a-5p的上游调控机制以及下游氧化应激和自噬二者相互之间的调控机制，本课题拟利用糖尿病小鼠动物模型，基于对环状RNA-circPDK1的表达干预，探讨其对miR-30a-5p的“海绵”作用，以及氧化应激和自噬活动之间相互影响的分子机制，完善上下游的网络调控关系，为糖尿病性白内障的防治提供新的干预靶点。

Oxidative stress and autophagy activity in lens epithelial cells (LECs) are involved in the pathogenesis of cataracts. Our previous study found that the expression of miR-30a-5p was decreased in LECs of diabetic cataracts. As a result of decreased expression of miR-30a-5p, the target gene TP53INP1 was negatively regulated to enhance oxidative stress; the target gene BECN1 was also negatively regulated to enhance autophagy; on the other hand, oxidative stress and autophagy of LECs show dynamic fluctuation and interaction in the persistent high glucose states . In order to understand the upstream regulatory mechanism of miR-30a-5p and the regulatory mechanism between oxidative stress and autophagy, our study intend to use the diabetic mouse model to probe into the “sponge” effect of miR-30a-5p and the molecular mechanism of interaction between oxidative stress and autophagy activity based on intervening into the expression of circRNA-circPDK1. Our study aims to provide new targets of intervention for the prevention and treatment of diabetic cataract.