Myostatin (GDF-8) as a key factor linking muscle mass and bone structure.
Myostatin (GDF-8) as a key factor linking muscle mass and bone structure.
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发表时间：
2010-03
影响因子：
1.9
通讯作者：
M. Elkasrawy;M. Hamrick
中科院分区：
文献类型：
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作者：
M. Elkasrawy;M. Hamrick
肌肉生长抑制素(GDF-8)是转化生长因子-β(TGF-β)超家族中的一员，在骨骼肌中高表达，其功能丧失可导致骨骼肌重倍增。肌肉抑制素基因缺陷小鼠已被用作研究肌肉-骨骼相互作用的模型，在这里我们回顾了与肌肉抑制素信号改变相关的骨骼表型。目前已知myostatin是间充质干细胞增殖和分化的关键调节因子，缺乏myostatin基因的小鼠表现为体脂减少，骨密度和强度普遍增加。在包括四肢、脊柱和颌骨在内的大多数解剖区域都可以观察到骨密度的增加，并且已经观察到肌肉生长抑制素抑制剂可以显著促进骨形成。肌肉生长抑制素在骨折愈合的早期也有表达，而肌肉生长抑制素缺乏会导致骨折骨痂大小和强度的增加。综上所述，这些数据表明，Myostatin对骨祖细胞的增殖和分化有直接影响，并且myostatin拮抗剂和抑制剂可能同时增强肌肉质量和骨强度。
Myostatin (GDF-8) is a member of the transforming growth factor-beta (TGF-beta) superfamily that is highly expressed in skeletal muscle, and myostatin loss-of-function leads to doubling of skeletal muscle mass. Myostatin-deficient mice have been used as a model for studying muscle-bone interactions, and here we review the skeletal phenotype associated with altered myostatin signaling. It is now known that myostatin is a key regulator of mesenchymal stem cell proliferation and differentiation, and mice lacking the myostatin gene show decreased body fat and a generalized increase in bone density and strength. The increase in bone density is observed in most anatomical regions, including the limbs, spine, and jaw, and myostatin inhibitors have been observed to significantly increase bone formation. Myostatin is also expressed in the early phases of fracture healing, and myostatin deficiency leads to increased fracture callus size and strength. Together, these data suggest that myostatin has direct effects on the proliferation and differentiation of osteoprogenitor cells, and that myostatin antagonists and inhibitors are likely to enhance both muscle mass and bone strength.