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.

Site Tools

  • AAAS
  • Subscribe
  • Feedback

Site Search

Search Advanced

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.

Abstract: The maintenance of adult skeletal muscle mass is ensured by physical exercise. Accordingly, physiological and pathological situations characterized by either impaired motor neuron activity, reduced gravity (microgravity during space flights), or reduced physical activity result in loss of muscle mass. Furthermore, a plethora of clinical conditions, including cancer, sepsis, diabetes, and AIDS, are associated with varying degrees of muscle atrophy. The cellular and molecular pathways responsible for maintaining the skeletal muscle mass are not well defined. Nonetheless, studies aimed at the understanding of 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).

Read the Full Text

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
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