肌肉是人体最大的器官和主要的能量代谢器官，保持一定的肌肉质量对于维持机体健康有重要意义。衰老导致终末分化的肌肉细胞中的蛋白质分解代谢显著增强，造成肌肉萎缩；同时衰老个体中的肌肉干细胞活性显著减弱，导致肌肉再生障碍。上述两方面的功能障碍共同造成了衰老导致的肌肉功能退化。本项目旨在阐明衰老诱导肌肉干细胞功能退化的表观遗传和转录调控机制，考察衰老对肌肉干细胞微环境的影响，鉴定导致衰老肌肉干细胞活性降低的关键基因，阐明衰老微环境调控这些关键基因表达的分子机制，解析衰老引发的肌肉萎缩降低肌肉干细胞活性的分子机制，为提高衰老个体的肌肉损伤修复能力提供新靶点、新策略。

Skeletal muscle is the largest organ in human body and is one of the major energy metabolism organs. Maintaining proper amount of muscle mass is important for survival and health aging. Aging induced muscle atrophy can accelerate the protein degradation in terminal differentiated muscle cells and lead to reduction of muscle mass. The activities of muscle stem cells are also impaired in aged muscle resulting in defects in muscle regeneration in aged population. Defects at the above two sides lead to muscle degeneration in aged population. This project aims to study the transcription and epigenetic regulation mechanism of aging induced muscle regeneration defects, identify the factors in aged microenvironment which impairs the functions of muscle stem cells. These studies will greatly facilitate the development of new strategy to treat aging induced muscle atrophy.