在载人航天尤其是中长期载人航天飞行中，失重导致的肌萎缩将影响航天员的健康与工作绩效，甚至危及航天任务的完成。但迄今为止仍缺乏行之有效的失重性肌萎缩实时监测与防治方法。在以往的研究中，我们发现尾悬吊模拟失重性肌萎缩形成过程中，小鼠血清循环miR-23a表达显著增高，且体外培养成肌细胞的回转器模拟失重性肌管萎缩也伴有明显的培养液中miR-23a增高。本课题拟进一步开展模拟失重性肌萎缩形成中：1）尾悬吊小鼠骨骼肌及血清循环miR-23a的动态变化规律及其差异性分析；2）尾悬吊小鼠血清循环miR-23a与失重性肌萎缩的相关性研究；3）头低位卧床人体血清循环miR-23a与模拟失重性肌萎缩的相关性验证；4）循环miR-23a与失重性肌萎缩相关性的作用机制研究。本研究将为进一步开展失重性肌萎缩的监测与防护方法研究提供新思路。

In long term space flight, weightlessness-induced muscle atrophy affects the health and work efficiency of astronauts, and even affect the completion of the space mission. So far we still lack effective real-time monitoring and control methods of muscle atrophy. In previous work, we preliminarily found that the circulating miR-23a was unregulated in the serum of mice and the medium of C2C12 cells using proven disuse muscular atrophy model. This paper intends to further develop: 1) the effects of disuse muscle atrophy on the expression of circulating miR-23a and miR-23a. 2) the correlation between circulating miR-23a and disuse muscle atrophy. 3) The study of the correlation between circulating miR-23a and human disuse muscle atrophy. 4) The mechanisms of the correlation between circulating miR-23a and weightlessness-induced muscle atrophy. This study will provide new ideas for further develop of muscle atrophy detection and protection measures .