腹主动脉瘤(AAA)尚无有效药物防治是临床治疗难点，其原因在于发生机制尚未阐明，既往我们研究发现与正常腹主动脉壁组织相比AAA瘤壁组织中LncRNA-Arg表达明显降低，并证实其可影响氧化应激通路，由于氧化应激影响Cathepsin S(Cat S)表达且Cat S促进AAA发展，我们提出假说:LncRNA-Arg通过调控氧化应激产物ROS生成影响Cat S表达抑制AAA的进展。本项目拟研究AAA患者与对照者间LncRNA-Arg、Cat S、氧化应激通路的变化情况，制作LncRNA-Arg重组载体转染至人平滑肌细胞及腹主动脉瘤小鼠模型中，观察其在平滑肌细胞中的作用机制及对小鼠动脉瘤血管的影响，以及Cat S结构变化、NADPH氧化酶、ROS、血管紧张素-Ⅱ与AAA发展的关系，从而验证LncRNA-Arg是AAA的一种内源性保护物质，本课题可能为AAA的发生提供新的作用机制和治疗靶点。

Abdominal aortic aneurysm (AAA) has not been prevented and treated by effective.drug, when the pathogenetic mechanism of AAA has not been clarified. But based on our previous research, by contrasted AAA artery wall tissue with normal artery wall tissue we found that the expression of LncRNA-Arg was obviously difference verified that can influence oxidative stress. At the same time Cathepsin S(Cat S) is likely to contribute to the occurrence of AAA while oxidative stress pathway affected the expression of Cat S theoretically. In view of that we hypothesized that LncRNA-Arg regulates the activity of Cat S by influenced the ROS generation of oxidative stress and inhibit AAA product progress finally. This project intends to make LncRNA–Arg recombinant vector transfection into SMCs and abdominal aortic aneurysm model in the mouse, to observe its effect on SMCs and vessel wall of mice aneurysm , and the Cat S structure change, NADPH oxidase activiton, ROS generation，Ang-Ⅱ and find the relationship between them and AAA, confirming LncRNA-Arg is an endogenous protective substance of AAA in the end. This project intends to provide new mechanism and therapeutic target for the occurrence of AAA.