胸主动脉腔内修复术（TEVAR）是B型夹层（TBAD）的首选术式，支架源性新破口(SINE)则是术后首位致死性并发症。课题组提出"支架源性损伤"是SINE主因的理论，并从力学角度获得了论证，据此指导了手术和支架改进，但SINE仍有发生，提示除力学机械损伤之外，锚定区主动脉发生不良重构可能也是SINE的重要成因。支架植入处的正常主动脉可观察到单核-巨噬细胞的浸润，而其浸润正是夹层主动脉的一大特点，也是TBAD的重要发病因素之一。因此，单核-巨噬细胞在支架锚定区主动脉内的浸润与极化可能是SINE的重要诱因。本申请将：明确SINE的发生伴随着单核-巨噬细胞浸润；明确机械力能调节单核-巨噬细胞在SINE处的浸润和极化；阐明机械力诱导SINE处单核-巨噬细胞调节的分子机制，为今后进一步研究其精细调节机制、发现新的药物干预靶点奠定基础。

Thoracic aortic endovascular repair (TEVAR) is currently the treatment of choice for Stanford B aortic dissection (TBAD), and the stent-graft induced new entry (SINE) is one of the most fatal complications of TEVAR. In our previous research, we proposed a hypothesis that mechanical injury induced by stent-graft implantation was the major cause of SINE. We furtherly proved this hypothesis from a purely mechanical point of view. Improved design of the stent-grafts and surgical strategies according to our previous study did decrease the risk of SINE, but there were still patients suffering from it. This suggested that poor remodeling of the dissected aorta under the abnormal mechanical force caused by the stent-grafts may be an important factor in the development of SINE. Stent-graft implantation can induce an inflammatory response characterized by monocyte-macrophage infiltration, which is also a significant feature of the dissected aorta and one of the most important causes of TBAD itself. Therefore, monocyte-macrophage infiltration and polarization at the site of SINE may be an important cause of it. In this program, we will try to prove the relevance between SINE and monocyte-macrophage infiltration; prove that the infiltration and polarization of monocyte-macrophage at the site of SINE can be regulated by mechanical forces; preliminary explore the molecular mechanism of monocyte-macrophage infiltration and polarization induced by mechanical force at the site of SINE. And finally, trying to lay the foundation for further research on more sophisticated regulation mechanisms and discover new drug intervention targets.