肌源性干细胞被称为是卫星细胞，骨骼肌受损后能够激活该细胞，起始增殖及分化再生出新的肌纤维。
研究发现，肌肉受损后，骨骼肌特异性microRNA miR-206在卫星细胞中明显上调，但是它在肌肉再生中的功能还不明确。
近日，美国德克萨斯大学西南医学中心的研究人员发现，在应答于肌肉损伤时，miR-206能够促进骨骼肌再生。相关论文发表在5月1日的The Journal of Clinical Investigation。
他们发现，在毒素损伤的老鼠模型，miR-206的敲除会延迟再生。此外，在杜兴氏肌肉营养不良的老鼠模型，miR-206的失去会加速并加重营养不良的表型。
而且，miR-206通过抑制一系列肌细胞生成的负调控因子，促进卫星细胞分化，并融合为肌肉纤维。
该研究表明，在骨骼肌再生时，miR-206对卫星细胞的分化具有决定性作用，而且miR-206能够延迟杜兴氏肌营养不良的进程，这对相关药物开发及疾病研究提供了新的思路。（生物谷Deepblue编译）
doi: 10.1172/JCI62656
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microRNA-206 promotes skeletal muscle regeneration and delays progression of Duchenne muscular dystrophy in mice
Ning Liu, Andrew H. Williams, Johanna M. Maxeiner, Svetlana Bezprozvannaya, John M. Shelton, James A. Richardson, Rhonda.
Skeletal muscle injury activates adult myogenic stem cells, known as satellite cells, to initiate proliferation and differentiation to regenerate new muscle fibers.The skeletal muscle–specific microRNA miR-206 is upregulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined.Here, we show that miR-206 promotes skeletal muscle regeneration in response to injury. Genetic deletion of miR-206 in mice substantially delayed regeneration induced by cardiotoxin injury.Furthermore, loss of miR-206 accelerated and exacerbated the dystrophic phenotype in a mouse model of Duchenne muscular dystrophy.We found that miR-206 acts to promote satellite cell differentiation and fusion into muscle fibers through suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and indicate that miR-206 slows progression of Duchenne muscular dystroph
