Induction of Cachexia in Mice by Systemically Administered Myostatin

By T. Zimmers, M. Davies, L. Koniaris, Paul Haynes, A. Esquela, K. Tomkinson, A. Mcpherron, N. Wolfman, Se-Jin Lee. Science, 2002

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Cellular and molecular mechanisms of muscle atrophy (2013, background): “Although an early report described severe (even fatal) atrophy when Chinese hamster ovary (CHO) cells engineered to express myostatin were injected into mouse skeletal muscle (Zimmers et al., 2002), these findings were not confirmed in transgenic mice.”
Myostatin Signals through a Transforming Growth Factor β-Like Signaling Pathway To Block Adipogenesis (2003, background): “Of note, systemic administration of myostatin to adult mice results in a cachexia-like syndrome that is associated with a profound loss of both muscle and fat (64).”
Cachexia: pathophysiology and clinical relevance. (2006, background): “Transgenic mice with the myostatin gene develop a cachexia-like syndrome that manifests with severe wasting (45).”
The molecular basis of skeletal muscle atrophy. (2004, background): “Systemic administration of this negative growth regulator leads to muscle wasting in mice (107), and treatment of cultured muscle cells with recombinant myostatin has resulted in the loss of protein and reduced protein synthesis rates (89).”
Reversal of cancer cachexia and muscle wasting by ActRIIB antagonism leads to prolonged survival. (2010, background): “Myostatin null mutations also lead to skeletal muscle hypertrophy in multiple species including humans, whereas forced myostatin overexpression in adult mice leads to systemic muscle wasting (Schuelke et al., 2004; Zimmers et al., 2002).”