期刊
SCIENCE
卷 296, 期 5572, 页码 1486-1488出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1069525
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资金
- NCI NIH HHS [5 T32 CA09139, R01 CA88866] Funding Source: Medline
- NICHD NIH HHS [R01 HD35887] Funding Source: Medline
Mice and cattle with genetic deficiencies in myostatin exhibit dramatic increases in skeletal muscle mass, suggesting that myostatin normally suppresses muscle growth. Whether this increased muscling results from prenatal or postnatal lack of myostatin activity is unknown. Here we show that myostatin circulates in the blood of adult mice in a latent form that can be activated by acid treatment Systemic overexpression of myostatin in adult mice was found to induce profound muscle and fat loss analogous to that seen in human cachexia syndromes. These data indicate that myostatin acts systemically in adult animals and may be a useful pharmacologic target in clinical settings such as cachexia, where muscle growth is desired.
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