一氧化碳释放分子-3(CORM-3)通过抑制晶状体上皮细胞凋亡对年龄相关性白内障治疗作用机制的研究

年龄相关性白内障（ARC）发病率高、致盲率高，手术是目前唯一有效的治疗方法。因手术医师匮乏、资源分布不均等导致中国白内障年手术率仅为发达国家的1/6。深入研究ARC发病机制，寻求有效的治疗药物，是当前急需解决的问题。本研究团队前期已在细胞水平证实一氧化碳释放分子-3（CORM-3）具有抗炎症和抗氧化应激等功能，且通过抑制晶状体上皮细胞（LECs）凋亡与ARC发病机制密切相关。据此我们提出假说：CORM-3可能通过抑制LECs凋亡而对白内障进行干预和治疗。本研究拟在成功构建与人ARC发展进程更为相似的小鼠模型基础上展开研究：揭示CORM-3抑制LECs凋亡的作用机制；明确CORM-3对白内障的治疗作用及其最佳剂量；确定CORM-3抑制LECs凋亡的关键功能基因和核心信号通路。通过本研究探索白内障药物治疗的可能性，对提高中国老年人的生存质量，减轻社会负担具有重要的科学意义。

The incidence rate and blindness rate of age-related cataract (ARC) are high. Surgery is the only effective treatment at present. Due to the shortage of surgeons and uneven distribution of resources, the annual cataract surgery rate in China is only 1/6 of that in developed countries. It is an urgent problem to study the pathogenesis of ARC and seek effective drugs.. Our team has confirmed that carbon monoxide release molecule-3 (CORM-3) has anti-inflammatory and anti-oxidation stress functions at cell level, and it is closely related to the pathogenesis of ARC by inhibiting the apoptosis of lens epithelial cells (LECs). Therefore, we propose the hypothesis that CORM-3 may intervene and treat cataract by inhibiting LECs apoptosis. Based on the successful construction of a mouse model which is more similar to human ARC, we want to explain the mechanism of CORM-3 inhibiting LECs apoptosis, clarify the therapeutic effect and the best dose of CORM-3 on cataract, determine the key functional genes and core signaling pathways of CORM-3 inhibiting LECs apoptosis. It is of great scientific significance to explore the possibility of drug treatment for cataract, which will improve the quality of life of the elderly and reduce the social burden in China.