年龄相关性白内障是老年人视力下降及致盲的主要原因，非手术靶向治疗将成为治疗白内障新的切入点。本项目组前期研究发现，Smac通过内质网应激途径诱导晶状体上皮细胞凋亡，且miR-29b和Smac在白内障晶状体组织中的表达呈负相关。通过生信分析发现lncRNA H19与miR-29可能存在直接结合位点且lncRNA H19在白内障晶状体组织中呈高表达，故提出假说：lncRNA H19可能作为ceRNA竞争性抑制miR-29，在转录后水平调控人晶状体上皮细胞中Smac基因的表达，参与白内障的发病过程。本课题拟于前期实验基础上，利用条件性基因敲除、RT-qPCR、荧光素酶报告基因系统等分子生物学技术，探讨H19/miR-29/Smac 轴在晶状体上皮凋亡中的作用，并通过细胞模型及动物实验验证下调lncRNA H19对白内障的抑制作用，为非编码RNA成为非手术治疗白内障的方式提供理论基础和实验依据。

Age-related cataract (ARC) is the main cause of decreased vision and blindness in the elderly. Thus, non-surgical targeted therapy will become a new entry point for the treatment of cataract. Our previous studies found that Smac induced apoptosis of lens epithelial cells via endoplasmic reticulum stress(ERS) pathway, and the expression of miR-29b and Smac was negatively correlated in cataract lens tissue. Through bioinformatic analysis, it was found that lncRNA H19 and miR-29 may have direct binding sites and lncRNA H19 is high-expression in cataract lens. Therefore, the hypothesis: lncRNA H19 may competitively inhibit miR-29 as ceRNA, regulate the expression of Smac gene in human lens epithelial cells at post-transcriptional level, and participate in the pathogenesis of cataract. Based on the previous experiments, this study aims to explore the role of H19/miR-29/Smac axis in lens epithelial apoptosis using molecular biology techniques such as conditional gene knockout, RT-qPCR, and luciferase reporter gene system. The inhibition of down-regulated lncRNA H19 on cataract will be verified by cell model and animal experiments, which is able to provide theoretical basis and experimental basis for making non-coding RNA a non-surgical treatment of cataract.