Induction of cachexia in mice by systemically administered myostatin
Induction of cachexia in mice by systemically administered myostatin
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DOI：
10.1126/science.1069525
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发表时间：
2002-05-24
期刊：
影响因子：
56.9
通讯作者：
Lee, SJ
中科院分区：
文献类型：
--
作者：
Zimmers, TA;Davies, MV;Lee, SJ
具有肌生长抑制素遗传缺陷的小鼠和牛表现出骨骼肌质量的显著增加，表明肌生长抑制素通常抑制肌肉生长。这种增加的肌肉是否是由于出生前或出生后缺乏肌肉生长抑制素活性的结果尚不清楚。在这里，我们表明，肌肉生长抑制素在成年小鼠的血液中循环，在一个潜在的形式，可以激活酸处理肌肉生长抑制素在成年小鼠的全身过度表达被发现诱导深刻的肌肉和脂肪损失类似于在人类恶病质综合征中看到的。这些数据表明，肌肉生长抑制素在成年动物中全身性地起作用，并且在需要肌肉生长的恶病质等临床环境中可能是有用的药理学靶点。
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.