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Am J Physiol Cell Physiol (April 8, 2009). doi:10.1152/ajpcell.00104.2009
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Submitted on March 6, 2009
Revised on March 30, 2009
Accepted on April 4, 2009

SMAD2 AND 3 TRANSCRIPTION FACTORS CONTROL MUSCLE MASS IN ADULTHOOD

Roberta Sartori1, Giulia Milan1, Maria Patron1, Cristina Mammucari1, Bert Blaauw1, Reimar Abraham1, and Marco Sandri2*

1 Venetian Institute of Molecular Medicine
2 University of Padova

* To whom correspondence should be addressed. E-mail: marco.sandri{at}unipd.it.

Loss of muscle mass occurs in a variety of diseases including cancer, chronic heart failure, AIDS, diabetes and renal failure, often aggravating pathological progression. Preventing muscle wasting by promoting muscle growth has been proposed as a possible therapeutic approach. Myostatin is an important negative modulator of muscle growth during myogenesis and myostatin inhibitors are attractive drug targets. However, the role of the myostatin pathway in adulthood and the transcription factors involved in the signaling are unclear. Moreover recent results confirm that other TGF{beta} members control muscle mass. Using genetic tools we perturbed this pathway in adult myofibers, in vivo, to characterize the downstream targets and their ability to control muscle mass. Smad2 and Smad3 are the transcription factors downstream of myostatin/TGF{beta} and induce an atrophy program which is MuRF1 independent and requires FoxO activity. Furthermore Smad2/3 inhibition promotes muscle hypertrophy independent of satellite cells but partially dependent of mTOR signalling. Thus myostatin and Akt pathways cross-talk at different levels. These findings point to myostatin inhibitors as good drugs to promote muscle growth during rehabilitation especially when they are combined with IGF1-Akt activators




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