CVMC的主要病理为MF，持续发展可致DCM，表现为顽固性心衰，预后极差。前期研究证实益气养阴、清心祛瘀的清心饮可促进PI3K-AKT信号通路传导明显抑制EndMT，但通路上游基因、蛋白等的调控机制尚待深入研究。晚近研究发现CXCL12/CXCR4生物学轴可调控PI3K-AKT通路传导，而CXCL12基因异常甲基化可下调CXCL12的表达水平。我们假说：清心饮可能通过干预CXCL12甲基化介导CXCL12/CXCR4生物学轴，进而调控PI3K-AKT信号通路来抑制CVMC中EndMT。本项目拟建立CVMC小鼠模型和细胞实验平台，探讨CVMC心肌纤维化EndMT过程中CXCL12基因甲基化介导CXCL12/CXCR4生物学轴对PI3K-AKT信号通路调控作用的同时，进一步观察清心饮的干预效应。项目完成将进一步阐明VMC心肌纤维化的病理机制以及清心饮治疗VMC的深层作用靶点，具有重要临床意义。

The main pathology of CVMC is MF, which can continue to develop to DCM, characterized by intractable heart failure with poor prognosis. Previous research has confirmed that Qingxinyin, which can nourish qi and yin and clear heart by removing stasis, can promote PI3K-AKT signaling pathway to significantly inhibit EndMT. However, the regulation mechanism of the gene and protein in the upstream of the pathway remains to be studied. Recent studies have found that CXCL12/CXCR4 biological axis can regulate PI3K-AKT pathway. Nevertheless, the abnormal methylation of CXCL12 gene can reduce the expression of CXCL12. We hypothesize that Qingxinyin may mediate the CXCL12/CXCR4 biological axis by interfering CXCL12 methylation, which then regulates the PI3K-AKT signaling pathway to suppress EndMT in CVMC. This project intends to establish a CVMC mouse model and a cell experiment platform to investigate the role of CXCL12 gene methylation mediated CXCL12/CXCR4 biological axis in the regulation of PI3K-AKT signaling pathway during the EndMT process of CVMC myocardial fibrosis, and further observe the intervention effect of Qingxinyin. The completion of the project will further elucidate the pathological mechanism of VMC myocardial fibrosis and the deep effect of Qingxinyin on the treatment of VMC, which is of great clinical significance.