骨骼肌不仅是运动系统的重要组成部分，在人体的代谢调控方面也起着关键的调节作用。骨骼肌的损伤再生及其质量稳态的维持都依赖于成肌细胞的增殖和相互融合。近期研究显示热激蛋白家族是调控骨骼肌稳态的重要信号系统，但其分子细胞机制尚有待深入。我们预实验发现肌肉损伤修复过程中热激蛋白Hsp90beta亚型的表达显著上调，进一步确认该蛋白调控成肌细胞增殖和组蛋白基因转录。此外，敲降Hsp90beta会导致组蛋白基体的重要调控分子NPAT在细胞核内解聚。在此基础上，我们计划深入研究Hsp90beta对组蛋白基体、组蛋白基因转录和成肌细胞增殖的调控机理；明确肌肉损伤修复中上调Hsp90beta的分子机制；并在小鼠体内干预Hsp90beta-NPAT信号通路，以确认该通路在体内肌肉再生中的作用。本研究将有助于明确成肌细胞增殖的分子机理，加深对骨骼肌再生调控规律的理解，为开发治疗肌肉相关疾病的新方法提供理论基础。

Skeletal muscle plays important roles in both physical performance and metabolism regulation. Muscle regeneration and homeostasis rely on the myoblast proliferation and fusion. Recent studies revealed that Heat Shock Protein family is critical for regulating muscle homeostasis, but the underlying mechanism is elusive. Here we found that Hsp90beta is significantly upregulated during muscle regeneration and it controls myoblast proliferation and histone transcription. Further, knockdown of Hsp90beta causes disruption of NPAT foci which is critical for modulating Histone Locus Body. We aim to further elucidate the mechanism for Hsp90beta to regulate Histone Locus Body, histone transcription, and myoblast proliferation; to explore the mechanism underlying the upregulation of Hsp90beta during muscle regeneration; and to reveal the in vivo roles of Hsp90beta-NPAT pathway in modulating muscle regeneration. Our study will not only help to delineating the mechanism underlying myoblast proliferation and muscle regeneration, but also provide theoretic basis for developing new treatment of muscle-related diseases.