废用性肌萎缩是延缓骨愈合及改建的重要因素，目前仍缺乏有效的干预措施。已知肌肉卫星细胞是修复损伤肌肉的关键细胞，其成肌分化基因的表达受启动子内H3组蛋白27位点赖氨酸三甲基化（H3K27me3）的负性调节。我们前期研究发现，镁离子（Mg2+）可显著拮抗肌肉萎缩，但具体机制不明；预实验初步证实Mg2+具有促进成肌分化基因表达、上调组蛋白去甲基化酶KDM6A及降低H3K27me3水平的作用，但具体理论构架有待进一步完善。为此，本研究拟通过分子生物学手段，首先阐明卫星细胞在废用性肌萎缩发生及恢复中的关键作用，初步明确Mg2+对卫星细胞生物学行为的影响；其次，探讨由KDM6A介导的H3K27me3去甲基化在卫星细胞成肌分化中的作用及机制;第三，明确Mg2+在上述途径中的作用，揭示其调控卫星成肌分化的具体分子机制。预期的研究结果将为Mg2+防治废用性肌萎缩的作用提供理论和实验依据，具有重要的临床意义。

Disused muscular atrophy is an important factor in delaying bone healing and remodeling, and there is still a lack of effective interventions for it. It is known that muscle satellite cells are the key cells to repair injured muscles whose myogenic differentiation genes expression is negatively regulated by lysine trimethylation located in the H3 histone 27 site (H3K27me3) in their promoters. In our previous studies, we found that Magnesium ions (Mg2+) could significantly antagonize muscular atrophy, but the specific mechanism was still unknown. Simultaneously, our preliminary experiments have initially confirmed that Mg2+ could promote the expression of myogenic differentiation genes, up-regulate histone demethylase KDM6A and reduce the level of H3K27me3, however, the specific theoretical framework needed to be further improved. Therefore, through some molecular biological means in this study, we will firstly clear the specific role of satellite cells in the progressive and recovery process of atrophic muscles and explore the effect of Mg2+ on its biological behavior. Further, the effect of H3K27me3 level in the myogenesis related gene promoter region mediated by KDM6A on the satellite cell myogenic differentiation will be detailedly investigated. Finally, the role of Mg2+ in the above pathways is clarified, and its specific molecular mechanism in satellite myoblast differentiation is also revealed. The expected results will provide theoretical and experimental basis for the prevention and treatment of disused muscular atrophy by Mg2+, which has important clinical significance.