目前腹主动脉瘤致病机制不清。血管平滑肌细胞表型的变化直接影响其正常功能。研究发现腹主动脉瘤中存在平滑肌细胞从收缩型向分泌型的表型转化，且干扰这种转化能够抑制腹主动脉瘤的发展。申请者已经证实腹主动脉瘤中出现mTORC1信号通路的异常活化，还证明了mTORC1信号通路调控VSMC表型的变化。因此提出假设，mTORC1信号通路调控的血管平滑肌细胞的表型转化可能是腹主动脉瘤的发病机制之一。希望通过应用mT/mG.Myh11CreERT2.Raptorflx/flx小鼠、mT/mG.Myh11CreERT2.Raptorflx/wt小鼠和mT/mG.Myh11CreERT2.Raptorwt/wt小鼠经三苯氧胺诱导在平滑肌细胞中特异性的敲除Raptor基因来阻断mTORC1信号通路，之后制作腹主动脉瘤模型以及细胞实验，来研究mTORC1信号通路在腹主动脉瘤中的作用。

The mechanism of abdominal aortic aneurysm isn’t clear. Phenotype switching of vascular smooth muscle cell has great influence to the function. Some studies find there is VSMC phenotype switching in abdominal aortic aneurysm and the growth of abdominal aortic aneurysm can be limited by inhibiting this kind of phenotype switching. The preliminary data from the applicant shows that there is abnormal activity of mTORC1 signaling pathway in abdominal aortic aneurysm and mTORC1 signaling pathway can regulate the phenotype switching. Our hypothesis is phenotype switching of VSMC, regulated by mTORC1 signaling pathway, is one of the mechanisms of abdominal aortic aneurysm. We would like to use mT/mG.Myh11-CreERT2.Raptor flx/flx mouse, mT/mG.Myh11- CreERT2.Raptor flx/wt mouse and mT/mG.Myh11- CreERT2.Raptor wt/wt mouse which can be induced Raptor ablation in VSMC specifically to study the function of mTORC1 signaling pathway in abdominal aortic aneurysm through in vivo model and in vitro experiments.