亲环素A（CyPA）通过其受体CD147分子作用于动脉粥样硬化发生、发展的全过程。其机制包括引起内皮细胞损伤、凋亡和活化所致的血管内皮功能障碍；趋化各种白细胞如中性粒细胞、嗜酸性粒细胞、单核/巨噬细胞、T淋巴细胞等聚集至炎症反应局部，并产生各类炎症因子，加重炎症反应；诱导巨噬细胞分泌基质金属蛋白酶，增强粥样斑块的不稳定性；介导巨噬细胞吞噬脂质形成泡沫细胞，加速脂质条纹形成；促进巨噬细胞、血管平滑肌细胞的增殖，引起血管壁增厚和重构等。对CyPA 与其受体CD147分子作用的研究可能为干预动脉粥样硬化提供新的方向。

Cyclophilin A (CyPA) participates in the whole development process of atherosclerosis through its receptor molecule CD147. During the process, cell injury, apoptosis and activation were caused, and dysfunction of endothelial cells emerged. The migration of leukocytes such as neutrophils, eosinophils, monocytes/macrophages and T lymphocytes to atherosclerotic lesions occurred, various inflammatory cytokines were produced, and inflammation was aggravated. The secretion of matrix metalloproteinases from macrophages was induced, and the instability of atheromatous plaques was increased. The formation of foam cells induced by macrophages' internalization of lipids was mediated, and the formation of fatty streaks was accelerated. Besides, the incrassation and reconstruction of vascular walls mediated by the proliferation of macrophages and vascular smooth muscle cells were promoted. Therefore, research on the roles of CyPA and CD147 may provide new directions for atherosclerosis intervention.