自噬功能失调是引起晶体蛋白凝集体形成、异常细胞器降解障碍以及细胞死亡增加的重要原因，其在白内障形成中的作用是近年研究的热点。我们前期研究发现：miR-30a和miR-204通过下调p53介导的细胞凋亡而抑制人老年性白内障形成过程中的氧化损伤；miR-30a、miR-100和miR-204在人透明晶状体上皮细胞和白内障上皮细胞有显著差异表达，在Emory小鼠中也存在一致性的差异表达；Beclin1、mTOR和MAP1LC3B分别是上述三种miRNA的预测靶基因。研究显示Beclin1、mTOR和MAP1LC3B是影响自噬水平的重要因子；而自噬与凋亡的通路又相互关联、互为调控。由此，本研究将检测人老年性白内障和其模型Emory小鼠晶状体组织中自噬功能失调情况，利用Emory小鼠的晶状体囊袋体外培养技术和体内模型，研究miR-30a、miR-100和miR-204在白内障中对自噬的网络调控机制。

Autophagy dysfunction causes cell death and accumulation of crystallin and damaged organelles, which are invested in cataract formation in recent years. According to our previous studies, miR-30a and miR-204 protect lens from oxidative damage in the progression of senile cataract by inhibiting p53-mediated apoptosis; miR-30a, miR-100 and miR-204 are the common part of microRNA differential expression profile of lens epithelium between senile cataract and normal tissues both in human and Emory mouse. The predicted target genes conclude Beclin1, mTOR and MAP1LC3B, respectively, which play import roles in autophagy process. And the dialogue between autophagy and cell apoptosis pathways influences cell’s normal functions and survival. In this study, we are going to invest the level of autophagy dysfunction in senile cataract tissues both in human and Emory mouse, and invest the role of miR-30a, miR-100 and miR-204 in regulating autophagy during senile cataract formation both in Emory mouse’s vitro (capsular bag cultivation) and vivo. We hope this study help to move forward a single step to understand the molecular mechanism of senile cataract.