失神经肌萎缩是周围神经损伤后运动功能丧失的主要原因，表现为肌细胞纤维化及萎缩。研究表明成肌调控是神经修复后功能恢复的限制因素，促进肌细胞分化及肌生成作用是预防失神经肌萎缩的关键，但机制尚不明确。我们前期工作已证实小鼠失神经肌萎缩过程中长链非编码RNA XLOC_015548的表达明显下调，细胞实验显示沉默/过表达XLOC_015548分别上调/下调靶基因Gadd45g表达，后者作为肌细胞负性调控因子将进一步抑制MyoD基因表达并最终影响肌细胞增殖与分化。因此，我们认为XLOC_015548可能通过介导Gadd45g/Myod调控失神经肌萎缩过程。本课题拟在细胞及动物水平，研究XLOC_015548/Gadd45g/Myod通路在肌细胞分化及肌生成过程中的调控作用，并验证该通路相关分子与失神经肌萎缩的关系，探索其对肌细胞成肌调控的影响与分子网络机制，以期为防治失神经肌萎缩提供新的理论依据。

Denervated muscle atrophy is the main cause of motor function loss after peripheral nerve injury, represent as myocytes fibrosis and atrophy. Studies have shown that the regulation of myogenesis is the limiting factor for function recovery after nerve repair, and the stimulation of myocytes differentiation and myogenesis is the key to preventing denervated muscle atrophy, but the mechanism is still unclear. Our previous work has confirmed that the expression of long non-coding RNA XLOC_015548 is significantly down-regulated during the progress of denervated muscle atrophy. Cell experiments have shown that silence/overexpress of XLOC_015548 would up-/down-regulate the target gene Gadd45g expression, which acts as a negative regulator of myocytes and further inhibit MyoD gene expression to affect myocyte proliferation and differentiation. Therefore, we believe that XLOC_015548 may regulate denervated muscle atrophy via Gadd45g/Myod. This project aims to explore the role of XLOC_015548/Gadd45g/Myod pathway in myocytes differentiation and myogenesis at cell and animal level, to verify the relationship between related molecules and denervated muscle atrophy, to explore the effect on myogenic regulation and the molecular network mechanism. In order to provide a new theoretical basis for the prevention and treatment of denervated muscle atrophy.