主动脉夹层是心血管领域高危的疾病之一，以血管炎症、细胞外基质降解为主要病理表现。中性粒细胞是最早到达病变部位的炎症细胞，中性粒细胞在主动脉夹层中聚集明显增加并通过释放多种活性物质促进主动脉夹层的发生、发展，消除中性粒细胞后主动脉夹层发生率可降低60%。预实验显示：在主动脉夹层患者和动物的外周血和夹层部位ADAMTS1水平升高；敲除ADAMTS1能抑制主动脉夹层的发生，减少血管壁中性粒细胞的浸润。为此我们提出假设，ADAMTS1通过介导中性粒细胞的多种功能参与主动脉夹层的发病。本项目拟通过动物模型和细胞实验的方法阐明ADMATS1对中性粒细胞功能的调控及其在主动脉夹层发病过程中的作用机制，寻找主动脉夹层可能的治疗靶点。

As one of the life-threatening diseases in cardiovascular system, aortic dissection is an extremely dangerous condition with a complex pathogenesis. Aortic dissection is associated with degeneration of the aortic media and inflammation cells infiltration. Neutrophils are key regulators of sterile vascular inflammation and are capable of secreting serine proteases, cathepsins, and reactive oxygen intermediates that can damage the extracellular matrix. In a mouse study, neutrophil depletion reduced the incidence of aortic dissection, suggesting that neutrophil recruitment is critical for the development of aortic dissection. In our preliminary experiments, the expression of ADAMTS1 protein increased in the peripheral blood and dissected tissues of patients and experimental animals, and ADAMTS1 knockout prevented aortic dissection development and neutrophils infiltration. Our present study aims to analyze the functions of ADAMTS1 in the pathogenesis of aortic dissection by regulating neutrophils, in order to explore possible new molecular mechanisms of aortic dissection．