心肌纤维化是心肌梗死后心脏重构的特征性病理改变，亦是导致心梗后心室功能恶化及顺应性降低的主要因素。研究表明，成纤维细胞向肌成纤维细胞转变（FMT）过程的失控是心梗后心肌广泛纤维化、心室恶性重塑形成的重要原因。我们课题组前期的研究揭示miR15b通过调控AKT3/eNOS抑制股动脉结扎后再血管化进程，而在探索miR15b与心肌梗死关系中发现，抑制miR15b的表达会加重心梗小鼠心肌纤维化程度，同时miR15b或许是通过影响下游FGF2靶基因的功能，参与到心肌成纤维细胞FMT过程当中。因此，本研究拟通过动物、细胞实验及临床分析，全面探明miR15b/FGF2通路对于心梗后FMT过程的影响及机制，力图从microRNA角度实现对心梗后过度FMT过程的有效抑制，为开发新型抗心肌纤维化药物提供新的靶点。

Myocardial fibrosis is a characteristic pathologic feature in cardiac remodeling process and also a critical component of ventricular dysfunction and reduced compliance after myocardial infarction. Studies demonstrated that the uncontrolled promotion of cardiac fibroblast to myofibroblast transition (FMT) greatly contributes to the massive myocardial fibrosis and malignant ventricular remodeling after myocardial infarction. Our previous studies have found that miR15b suppressed the revascularization progress after femoral artery ligation through regulating AKT3/eNOS pathway. While during the observation of the relationship between miR15b and myocardial infarction, we have found that inhibition of miR15b expression increased the degree of myocardial fibrosis in mice after myocardial infarction, and meanwhile miR15b probably participated in the FMT course of cardiac fibroblasts via affecting its downstream target gene FGF2. So, in this study we plan to systemically reveal the action of miR15b/FGF2 pathway in the FMT course and its mechanism, and attempt to realize the effective control of the excessive FMT from the aspect of epigenetic regulation, for providing a new treating target to develop the new anti-myocardial fibrotic drugs.