Elkasrawy M N, Hamrick M W
Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, GA 30912, USA.
J Musculoskelet Neuronal Interact. 2010 Mar;10(1):56-63.
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.
肌生成抑制素（生长分化因子8）是转化生长因子-β（TGF-β）超家族的成员，在骨骼肌中高度表达，肌生成抑制素功能丧失会导致骨骼肌质量加倍。肌生成抑制素缺陷小鼠已被用作研究肌肉与骨骼相互作用的模型，在此我们综述与肌生成抑制素信号改变相关的骨骼表型。现在已知肌生成抑制素是间充质干细胞增殖和分化的关键调节因子，缺乏肌生成抑制素基因的小鼠体脂减少，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观察到骨密度增加，并且已观察到肌生成抑制素抑制剂可显著增加骨形成。肌生成抑制素也在骨折愈合的早期阶段表达，肌生成抑制素缺乏会导致骨折痂大小和强度增加。总之，这些数据表明肌生成抑制素对骨祖细胞的增殖和分化有直接影响，并且肌生成抑制素拮抗剂和抑制剂可能会增加肌肉质量和骨骼强度。
