动脉粥样硬化（AS）的发生发展与炎症反应密切相关，我们前期研究发现颈动脉粥样硬化狭窄患者血清和斑块内的炎症因子YKL-40表达均明显增高，斑块内的表达与巨噬细胞分布一致，且血清的表达水平与斑块稳定性呈负相关。研究表明巨噬细胞的作用贯穿于AS过程，其能否及时有效清除凋亡细胞为主的坏死核心是维持斑块稳定性的重要环节，而巨噬细胞的胞葬作用正是一个吞噬清除凋亡细胞的过程，因而，巨噬细胞的胞葬功能可能在AS斑块稳定中具有重要作用。我们进一步研究发现，YKL-40刺激巨噬细胞后其胞葬功能减弱，且极化表型可能受到影响。因此，本项目拟进一步明确YKL-40是否通过调控巨噬细胞的胞葬功能和极化表型等机制，影响AS斑块的稳定性。本项目将为探讨AS的发生发展机制提供新思路，甚至为AS斑块稳定性研究提供可能的干预靶点。

The occurrence and development of atherosclerosis (AS) are closely related to the inflammatory response. Our previous study found that the expression of inflammatory cytokine YKL-40 in sera and plaques of patients with carotid atherosclerosis were significantly increased. Meanwhile, the expression of YKL-40 in the plaques was consistent with the distribution of the macrophages, and the expression level in serum was negatively correlated with the stability of the plaques. Studies have shown an important role of macrophages throughout the AS process. Timely and effective removal of apoptotic cell-based necrotic core by macrophages is an important part of the maintenance of plaque stability, and the efferocytosis of macrophage cell is a process of phagocytosis and clearance of apoptotic cells. Therefore, the efferocytosis of macrophages may play an important role in the stability of AS plaque. Our further study found that the efferocytosis of macrophages was weakened after YKL-40 stimulation, and the polarized phenotype may be affected as well. Therefore, this project intends to further clarify whether YKL-40 affects the stability of AS plaques by regulating the efferocytosis of macrophage and polarization phenotype. This project will provide new ideas for exploring the mechanism of the occurrence and development of AS and even provide possible intervention targets for the study of AS plaque stability.