川崎病(KD)冠状动脉损伤已成为儿童最常见的获得性心脏疾病，其典型特征为大量巨噬细胞浸润的增生性炎症，巨噬细胞和淋巴细胞的异常激活被认为与血管损伤形成密切相关。我们研究发现血管内皮细胞的Ca2+/CaN-NFAT信号通路参与KD冠状动脉损伤的发生发展。并也发现巨噬细胞Ca2+/CaN-NFAT信号通路与KD冠状动脉损伤有关。本项目拟通过建立免疫性冠状动脉损伤模型，对巨噬细胞中Ca2+/CaN-NFAT信号通路在免疫性冠状动脉损伤和修复中的作用及机制进行研究。观察巨噬细胞中Ca2+/CaN-NFAT信号过表达和敲低后与免疫性冠状动脉损伤及修复之间的关系，以说明巨噬细胞中Ca2+/CaN-NFAT信号通路对免疫性冠状动脉损伤的调控作用。同时给予CaN抑制剂干预，研究抑制巨噬细胞Ca2+/CaN-NFAT信号通路是否可以改善免疫性冠状动脉损伤的修复。

Coronary artery lesions (CALS) in Kawasaki disease (KD) have become the most common acquired heart disease in children. It is typically characterized by proliferative inflammation of macrophage infiltration. Abnormal activation of macrophages and lymphocytes is thought to be closely related to CALs. Our previous study found that the Ca2+/CaN-NFAT signaling pathway of vascular endothelial cells participates in the development of CALs in KD, macrophage Ca2+/CaN-NFAT signaling pathway was associated with CALs in KD. This study aims to investigate the effects and mechanism of macrophage Ca2+/CaN-NFAT signaling pathway in immune CALs and repair by establishing a model of immune CALs. We intend to clarify the regulative effects of macrophage Ca2+/CaN-NFAT signaling pathway for immune CALs by observing the relationship between macrophage Ca2+/CaN-NFAT signal overexpression and knockdown and immune CALs and repair. At the same time, CaN inhibitors are given to investigate whether inhibition of macrophage Ca2+/CaN-NFAT signaling pathway can improve the repair of immune CALs.