Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Subscribe

Sci. STKE, 3 August 2004
Vol. 2004, Issue 244, p. re11
[DOI: 10.1126/stke.2442004re11]

REVIEWS

Molecular and Cellular Determinants of Skeletal Muscle Atrophy and Hypertrophy

Vittorio Sartorelli* and Marcella Fulco

Muscle Gene Expression Group Laboratory of Muscle Biology, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.

Gloss: This STKE Review with two figures and 133 references discusses the signaling pathways that are implicated in both building muscle and losing muscle. Protein degradation pathways are activated in response to lack of muscle use, which leads to muscle atrophy. Muscle hypertrophy in response to exercise involves both changes in gene expression and protein activities in the existing myofibers and recruitment of satellite cells to increase myofiber numbers. Studies aimed at understanding the mechanisms underlying either muscular atrophy or hypertrophy have begun to identify the physiological determinants and clarify the molecular pathways responsible for the maintenance of muscle mass.

*Corresponding author. E-mail: sartorev{at}mail.nih.gov

Citation: V. Sartorelli, M. Fulco, Molecular and Cellular Determinants of Skeletal Muscle Atrophy and Hypertrophy. Sci. STKE 2004, re11 (2004).


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
Cellular and molecular mechanisms of muscle atrophy.
P. Bonaldo and M. Sandri (2013)
Dis. Model. Mech. 6, 25-39
   Abstract »    Full Text »    PDF »
Muscle-specific overexpression of NCOATGK, splice variant of O-GlcNAcase, induces skeletal muscle atrophy.
P. Huang, S.-R. Ho, K. Wang, B. C. Roessler, F. Zhang, Y. Hu, D. B. Bowe, J. E. Kudlow, and A. J. Paterson (2011)
Am J Physiol Cell Physiol 300, C456-C465
   Abstract »    Full Text »    PDF »
Whey and casein labeled with L-[1-13C]leucine and muscle protein synthesis: effect of resistance exercise and protein ingestion.
S. Reitelseder, J. Agergaard, S. Doessing, I. C. Helmark, P. Lund, N. B. Kristensen, J. Frystyk, A. Flyvbjerg, P. Schjerling, G. van Hall, et al. (2011)
Am J Physiol Endocrinol Metab 300, E231-E242
   Abstract »    Full Text »    PDF »
Smad2 and 3 transcription factors control muscle mass in adulthood.
R. Sartori, G. Milan, M. Patron, C. Mammucari, B. Blaauw, R. Abraham, and M. Sandri (2009)
Am J Physiol Cell Physiol 296, C1248-C1257
   Abstract »    Full Text »    PDF »
Inhibition of Myoblast Differentiation by Tumor Necrosis Factor {alpha} Is Mediated by c-Jun N-terminal Kinase 1 and Leukemia Inhibitory Factor.
J. Alter, D. Rozentzweig, and E. Bengal (2008)
J. Biol. Chem. 283, 23224-23234
   Abstract »    Full Text »    PDF »
Rapamycin inhibits the growth and muscle-sparing effects of clenbuterol.
W. O. Kline, F. J. Panaro, H. Yang, and S. C. Bodine (2007)
J Appl Physiol 102, 740-747
   Abstract »    Full Text »    PDF »
Bidirectional regulation of upstream IGF-I/insulin receptor signaling and downstream FOXO1 in cardiomyocytes.
T.-J. Liu, H.-C. Lai, C.-T. Ting, and P. H Wang (2007)
J. Endocrinol. 192, 149-158
   Abstract »    Full Text »    PDF »
Measuring body composition in chronic heart failure: A comparison of methods.
N. H.M.K. Uszko-Lencer, F. Bothmer, P. E.J. van Pol, and A. M.W.J. Schols (2006)
Eur J Heart Fail 8, 208-214
   Abstract »    Full Text »    PDF »
Proteome Dynamics during C2C12 Myoblast Differentiation.
T. Kislinger, A. O. Gramolini, Y. Pan, K. Rahman, D. H. MacLennan, and A. Emili (2005)
Mol. Cell. Proteomics 4, 887-901
   Abstract »    Full Text »    PDF »

To Advertise     Find Products


Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882