Role of glucocorticoids in the molecular regulation of muscle wasting

Michael Menconi*, Moin Fareed, Patrick O'Neal, Vitaliy Poylin, Wei Wei, Per Olof Hasselgren

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

90 Scopus citations


OBJECTIVE: To review glucocorticoid-regulated molecular mechanisms of muscle wasting. DESIGN: Review of recent literature describing the role of glucocorticoids in the regulation of proteolytic mechanisms, transcription factors, and nuclear cofactors in skeletal muscle during various catabolic conditions. MAIN RESULTS: Catabolic doses of glucocorticoids induce muscle atrophy both in vivo and in vitro by stimulating protein breakdown and inhibiting protein synthesis. Signaling pathways that regulate muscle protein synthesis at the translational level are inhibited by glucocorticoids. Glucocorticoids increase the expression and activity of the ubiquitin-proteasome pathway, a major proteolytic mechanism of muscle atrophy. The expression and activity of muscle wasting-related transcription factors, including C/EBPβ and δ and Forkhead box O 1, 3, and 4, as well as the nuclear cofactor p300, are up-regulated by glucocorticoid excess. CONCLUSIONS: Muscle wasting in various catabolic conditions is, at least in part, regulated by glucocorticoids. The role of glucocorticoids in muscle wasting is complex and reflects regulation at the molecular level of multiple mechanisms influencing both synthesis and degradation of muscle proteins.

Original languageEnglish (US)
Pages (from-to)S602-S608
JournalCritical care medicine
Issue number9 SUPPL.
StatePublished - Sep 2007


  • Glucocorticoids
  • Muscle wasting
  • Nuclear cofactors
  • Transcription factors
  • Ubiquitin-proteasome pathway

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine


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