肠道微生物降解高脂饮食后FMO3酶合成TMAO是动脉粥样硬化(AS）发病重要机制，整合了基因信息和CT影像学数据的模型将为AS早期风险预警提供参考。项目前期发现位于FMO3 3’UTR区的rs41272509[A/G]位点与AS风险相关，该位点位于miR-340-5p与FMO3 mRNA的结合位置，影响FMO3的表达水平。假设rs41272509位点通过影响miR-340-5p与FMO3 mRNA结合从而调节FMO3酶表达和活性，参与胆碱-TMA-TMAO代谢途径，影响胆固醇代谢和巨噬细胞活性，从而参与AS发生发展过程。项目将从细胞和动物层次探索rs41272509通过miR-340-5p影响FMO3表达和活性的作用与机制，并整合CT数据与miR-340-5p、rs41272509和TMAO含量的血液数据建立用于评估蒙古族人群罹患AS风险的综合模型，为揭示AS发病机制和风险预警提供新思路。

The synthesis of TMAO by FMO3 is one of the most important mechanisms of the pathogenesis of atherosclerosis (AS) after gut microbiota degrading high-fat diet. The model integrating gene information and CT imaging data will provide a reference for early warning of AS. In the previouswork, the rs41272509 [A/G] locus in the 3'UTR region of FMO3 was found to be associated with the risk of AS, which was located at the binding site of miR-340-5p and FMO3 mRNA,affecting FMO3 expression. Thus we propose the following scientific hypothesis: rs41272509 regulates FMO3 enzyme expression and activitysite by affecting miR-340-5p and FMO3 mRNA binding, involved in choline-TMA-TMAO metabolic pathway and affecting cholesterol metabolism and macrophage activity, and thus participate in the AS The development. The project will explore the role and mechanism of rs41272509 on the expression and activity of FMO3 through miR-340-5p at the cellular and animal level and integrate the CT imaging data with the blood data of miR-340-5p, rs41272509 and TMAO content for the assessment of Mongolia population suffering from the risk of AS model to reveal the pathogenesis of AS and risk warning provide new ideas.