老年性白内障的发生与伴随衰老的氧化应激损伤密切相关，近年研究发现miRNAs参与了老年性白内障的发病机制。我们的前期工作中发现老年性白内障晶状体上皮细胞相对正常人的miR-204表达显著降低，并且生物信息学分析发现miR-204可作用于TXNIP的3′ UTR区，抑制TXNIP表达；同时也可作用于ALDH1A3/TF的TATA-box区，促进ALDH1A3/TF转录，以此调节氧化损伤相关基因表达并影响白内障发生。本研究拟在前期发现的基础上通过荧光素酶报告基因系统以及动物实验等方法，进一步确证miR-204与TXNIP的3′ UTR及ALDH1A3/TF的TATA-box区互补结合的分子机制，以及在白内障动物模型中观察miR-204是否能影响白内障的形成。最终阐明miR-204通过两种机制调节氧化应激相关靶基因，并参与白内障形成的分子机制，从而为白内障的防治提供理论基础和新的药物干预靶点。

Senile cataract is closely related to oxidative stress accompanied by senescence. Recently, it has been found miRNAs are also involved in senile cataractogenesis. Our previous work suggested the expression of miR-204 was significantly decreased in cataract lens epithelial cells than their healthy counterparts. Furthermore, bioinformatics analysis showed miR-204 could bind to the 3′ UTR region of TXNIP and repress its expression; Meanwhile, miR-204 could also bind to the TATA-box region of ALDH1A3/TF and promote their transcription. These regulated oxidative stress related genes may contribute to cataract formation. Our study aims to confirm the specific binding of miR-204 and the 3′ UTR of TXNIP and the TATA-box region of ALDH1A3/TF and their molecular mechanisms in luciferase reporter system; Also we would observe the effect of miR-204 on cataract formation in cataract animal models through animal experiments. Eventually we would clarify the molecular mechanism of miR-204 induced regulation of oxidative stress related genes and subsequent cataract formation through two distinct mechanisms. Our study could provide with theoretical basis of the prevention and treatment of cataract and new targets for novel therapeutic interventions.