人肌纤生成调节因子1（MR-1）是课题组前期工作发现的新功能基因，它高表达于横纹肌并定位于肌原纤维，表达上调时明显促进肌节分子F-actin、MLC-2等快速组装并明显上调。以肌节组装为基础的肌原纤维生成是心肌细胞分化的关键环节，MR-1可能通过调节肌节组装影响心肌细胞的分化。为证实这一假说，本研究拟在大鼠心肌成肌细胞系H9c2分化的模型中探明 MR-1对肌节组装的调节作用，证实：①H9c2血清饥饿诱导分化过程中MR-1的表达变化；②MR-1过表达或沉默对H9c2血清饥饿诱导分化的影响；③MR-1在Ca2+/MLCK/MLC-2v/F-actin肌纤生成信号途径中的作用。该研究的完成将为心脏发育、分化和重塑机制的阐明提供有力的理论支持，也将为心肌损伤、心肌肥大、心力衰竭等疾病的防治提供有效的干预靶点。

Human myofibrillogenesis regulator 1 (hMR-1) is a novel characterized human functional gene cloned by our research group. MR-1 is highly expressed in myocardium and skeletal muscle, locating on the myofibrils. Upregulation of MR-1 promotes rapid sarcomere organization and upregulation of critical sarcomeric proteins such as F-actin and MLC-2. Myofibrillogenesis, a highly ordered and precise organization of sarcomeres, is critical for differentiation of cardiomyocyte. MR-1 may influence the differentiation of cardiomyocyte by regulating sarcomere organization. To verify this hypothesis, we investigated in H9c2 (the heart embryonic myoblast) differentiation model and explored the possible molecular mechanism with the following points: 1) MR-1 expressions in the process of H9c2 differentiation induced by serum-starvation, 2) overexpressed- or silenced-MR-1's influence in the differentiation process of serum-starved H9c2, 3) The role of MR-1 in the Ca2+/MLCK/MLC-2v/F-actin mediated signaling pathway specifically in the myofibrillogenesis. The result of our research may provide powerful theoretical support for defining the mechanism of cardiac development, differentiation and remodeling, as well as therapeutic targets for both prevention and treatment of myocardium injury, cardiac hypertrophy and heart failure.