Myology Laboratory, Institute of Biomedical Problems RAS, Moscow 123007, Russia.
Int J Mol Sci. 2020 Oct 26;21(21):7940. doi: 10.3390/ijms21217940.
Skeletal muscle fibers have a unique capacity to adjust their metabolism and phenotype in response to alternations in mechanical loading. Indeed, chronic mechanical loading leads to an increase in skeletal muscle mass, while prolonged mechanical unloading results in a significant decrease in muscle mass (muscle atrophy). The maintenance of skeletal muscle mass is dependent on the balance between rates of muscle protein synthesis and breakdown. While molecular mechanisms regulating protein synthesis during mechanical unloading have been relatively well studied, signaling events implicated in protein turnover during skeletal muscle recovery from unloading are poorly defined. A better understanding of the molecular events that underpin muscle mass recovery following disuse-induced atrophy is of significant importance for both clinical and space medicine. This review focuses on the molecular mechanisms that may be involved in the activation of protein synthesis and subsequent restoration of muscle mass after a period of mechanical unloading. In addition, the efficiency of strategies proposed to improve muscle protein gain during recovery is also discussed.
骨骼肌纤维具有独特的能力，可以根据机械负荷的变化来调节其代谢和表型。事实上，慢性机械负荷会导致骨骼肌质量增加，而长时间的机械卸载会导致肌肉质量显著下降（肌肉萎缩）。骨骼肌质量的维持取决于肌肉蛋白合成和分解速率之间的平衡。虽然在机械卸载过程中调节蛋白合成的分子机制已经得到了相对较好的研究，但在骨骼肌从卸载中恢复过程中涉及到的蛋白周转的信号事件还没有得到很好的定义。更好地理解在废用性萎缩引起的肌肉质量恢复过程中潜在的分子事件，对于临床和太空医学都具有重要意义。本综述重点介绍了在机械卸载后，可能参与蛋白合成激活以及随后恢复肌肉质量的分子机制。此外，还讨论了在恢复过程中提高肌肉蛋白获得效率的策略的有效性。
