Induction of cachexia in mice by systemically administered myostatin

Teresa A. Zimmers, Monique V. Davies, Leonidas G. Koniaris, Paul Haynes, Aurora F. Esquela, Kathy N. Tomkinson, Alexandra C. McPherron, Neil M. Wolfman, Se Jin Lee

Research output: Contribution to journalArticle

650 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)1486-1488
Number of pages3
JournalScience
Volume296
Issue number5572
DOIs
StatePublished - May 24 2002

ASJC Scopus subject areas

  • General

Fingerprint Dive into the research topics of 'Induction of cachexia in mice by systemically administered myostatin'. Together they form a unique fingerprint.

  • Cite this

    Zimmers, T. A., Davies, M. V., Koniaris, L. G., Haynes, P., Esquela, A. F., Tomkinson, K. N., McPherron, A. C., Wolfman, N. M., & Lee, S. J. (2002). Induction of cachexia in mice by systemically administered myostatin. Science, 296(5572), 1486-1488. https://doi.org/10.1126/science.1069525