动脉粥样硬化是导致心血管病、中风等疾病死亡的重要病理原因，是国内外重大的公共卫生问题。炎症参与动脉粥样硬化斑块形成的所有过程，但是其调控机制还不清楚。本项目探索巨噬细胞膜受体蛋白SHPS-1在动脉粥样硬化发生过程中的调控作用。前期研究显示SHPS-1的表达与动脉粥样硬化发生及巨噬细胞的泡沫化有正相关性。在SHPS-1基因敲除小鼠模型中，观察到SHPS-1敲除能阻止动脉粥样硬化斑块的形成。在前期研究基础上我们提出假设，SHPS-1通过调节巨噬细胞的功能来调控动脉粥样硬化斑块形成。本项目中我们将通过研究SHPS—1对巨噬细胞迁移，泡沫化，极化等进程的调控来探索SHPS-1对巨噬细胞功能的调控。其次筛选SHPS-1的靶蛋白和受调控信号通路探索SHPS-1对动脉粥样硬化调控。最后根据SHPS-1靶蛋白的挽救实验探索SHPS-1对动脉粥样硬化的新调控机制，使临床上对动脉硬化的治疗策略开辟出有效方法。

Atherosclerosis is the major pathological cause of death from cardiovascular disease，stroke and it becomes an important public health problem worldwide. Inflammation is involved in all stages of atherosclerotic plaque formation, but the underlying mechanism remains unclear. This project explores the role of macrophage membrane receptor protein SHPS-1 in the development of atherosclerosis. Previous studies have shown that the expression of SHPS-1 is positively associated with the occurrence of atherosclerosis and macrophage foaming. It was observed that SHPS-1 can prevent atherosclerosis development in gene knockout mouse model. We hypothesized that SHPS-1 regulates atherosclerotic plaque formation by regulating the function of macrophages. In project, we will study the regulation of SHPS-1 on macrophage by dissecting the macrophage migration, foaming, polarization processes. Secondly, we will screen target proteins and signaling pathways regulated by SHPS-1 to explore the molecular mechanism of SHPS-1 in atherosclerosis. Finally, we will test SHPS-1 target protein rescue efficient to provide a new possible therapeutic strategy for atherosclerosis.