心肌纤维化是多种心血管疾病的终末期表现，成纤维细胞(CFB)转分化是其主要病理基础。课题组前期研究发现c-SKI与TGF-β通路存在双向调控，共同调节CFB转分化，同时lncRNA、miRNA又可靶向c-SKI参与心肌纤维化进程，但具体机制不明。因而本课题基于芯片数据、生物信息学分析和预实验，提出假说TGF-β介导lncRNATerc表达，而Terc结合转录因子MYC下调c-SKI表达，加速CFB转分化。本研究通过观察小鼠和人原代CFB转分化过程中lncRNATerc的表达变化，TGF-β与lncRNATerc、lncRNATerc与c-SKI间的靶向关系，探讨其对CFB转分化的影响。同时建立心肌纤维化动物模型，观察lncRNATerc对心脏结构、心肌组织形态及相关蛋白表达的影响，阐明其作用机制，探讨lncRNATerc作为改善纤维化有效靶点的可能，为心肌纤维化的防治提供新思路。

Cardiac fibrosis is a pathological feature at the end stage of some cardiovascular diseases and cardiac fibroblasts (CFB) transdifferentiation is the main pathological basis. Previous studies have found that there is a two-way regulation between c-SKI and TGF-β pathway, which regulates CFB transdifferentiation, and lncRNA, miRNA can be targeted c-SKI to participate in the process of myocardial fibrosis,but the specific mechanism is unknown. Therefore, by analyzing chip data, bioinformatics analysis and preliminary experiments, it is proposed that TGF-β mediates lncRNA Terc expression, while Terc binds to transcription factor MYC, down-regulates c-SKI expression, and accelerates CFB transdifferentiation. This study was to investigate the expression of lncRNA Terc during the transdifferentiation of mouse and human primary CFB, the targeting relationship between TGF-β and lncRNA Terc, lncRNA Terc and c-SKI and its effect on transdifferentiation. In addition, we also investgate the effect of lncRNATerc on structure of heart,myocardial tissue morphology and protein expression related to myocardial fibrosis in animal model of myocardial fibrosis to clarify the underlying mechanisms. These studies are designed to explore the possibility of lncRNA Terc as a effective target for Improving fibrosis, to provide new ideas for its prevention and treatment of myocardial fibrosis.