Abstract
Myostatin (GDF-8) is a member of the transforming growth factor-beta (TGF-β) 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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 56-63 |
| Number of pages | 8 |
| Journal | Journal of Musculoskeletal Neuronal Interactions |
| Volume | 10 |
| Issue number | 1 |
| State | Published - Mar 1 2010 |
Fingerprint
Keywords
- ActRIIB
- Bone density
- GDF-8
- Hypertrophy
- Muscle-bone interactions
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism
- Physiology
- Orthopedics and Sports Medicine
Cite this
Myostatin (GDF-8) as a key factor linking muscle mass and bone structure. / Elkasrawy, Moataz N.; Hamrick, Mark W.
In: Journal of Musculoskeletal Neuronal Interactions, Vol. 10, No. 1, 01.03.2010, p. 56-63.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Myostatin (GDF-8) as a key factor linking muscle mass and bone structure
AU - Elkasrawy, Moataz N.
AU - Hamrick, Mark W
PY - 2010/3/1
Y1 - 2010/3/1
N2 - Myostatin (GDF-8) is a member of the transforming growth factor-beta (TGF-β) 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.
AB - Myostatin (GDF-8) is a member of the transforming growth factor-beta (TGF-β) 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.
KW - ActRIIB
KW - Bone density
KW - GDF-8
KW - Hypertrophy
KW - Muscle-bone interactions
UR - http://www.scopus.com/inward/record.url?scp=77649198629&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=77649198629&partnerID=8YFLogxK
M3 - Review article
C2 - 20190380
AN - SCOPUS:77649198629
VL - 10
SP - 56
EP - 63
JO - Journal of Musculoskeletal Neuronal Interactions
JF - Journal of Musculoskeletal Neuronal Interactions
SN - 1108-7161
IS - 1
ER -