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Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction
Science ( IF 56.9 ) Pub Date : 2021-10-15 , DOI: 10.1126/science.abe5620
William Roman 1, 2 , Helena Pinheiro 2 , Mafalda R Pimentel 2 , Jessica Segalés 1 , Luis M Oliveira 2 , Esther García-Domínguez 3 , Mari Carmen Gómez-Cabrera 3 , Antonio L Serrano 1 , Edgar R Gomes 2 , Pura Muñoz-Cánoves 1, 4, 5
Affiliation  

Regeneration of skeletal muscle is a highly synchronized process that requires muscle stem cells (satellite cells). We found that localized injuries, as experienced through exercise, activate a myofiber self-repair mechanism that is independent of satellite cells in mice and humans. Mouse muscle injury triggers a signaling cascade involving calcium, Cdc42, and phosphokinase C that attracts myonuclei to the damaged site via microtubules and dynein. These nuclear movements accelerate sarcomere repair and locally deliver messenger RNA (mRNA) for cellular reconstruction. Myofiber self-repair is a cell-autonomous protective mechanism and represents an alternative model for understanding the restoration of muscle architecture in health and disease.

中文翻译:

生理损伤后的肌肉修复依赖于细胞重建的核迁移

骨骼肌的再生是一个高度同步的过程,需要肌肉干细胞(卫星细胞)。我们发现,通过运动体验到的局部损伤会激活一种独立于小鼠和人类卫星细胞的肌纤维自我修复机制。小鼠肌肉损伤触发涉及钙、Cdc42 和磷酸激酶 C 的信号级联反应,通过微管和动力蛋白将肌核吸引到受损部位。这些核运动加速肌节修复并局部递送信使 RNA (mRNA) 用于细胞重建。肌纤维自我修复是一种细胞自主保护机制,代表了一种用于理解健康和疾病中肌肉结构恢复的替代模型。
更新日期:2021-10-14
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