期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 13, 期 4, 页码 423-428出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0b013e32833a5107
关键词
CCAAT/enhancer-binding protein beta; Forkhead box O 1; glucocorticoids; histone deacetylases; muscle wasting; MyoD; myogenin; p300
资金
- NIH [R01 DK37908, R01 NR08545]
- Department of Clinical Medicine, 'Sapenza', University of Rome, Rome, Italy
Purpose of review The purpose of this review is to discuss novel insight into mechanisms of glucocorticoid-regulated muscle wasting, in particular the role of transcription factors and nuclear cofactors. In addition, novel strategies that may become useful in the treatment or prevention of glucocorticoid-induced muscle wasting are reviewed. Recent findings Studies suggest that glucocorticoid-induced upregulation of the transcription factors Forkhead box O 1 and CCAAT/enhancer-binding protein beta and downregulation of MyoD and myogenin are involved in glucocorticoid-induced muscle wasting. In addition, glucocorticoid-induced hyperacetylation caused by increased expression of the nuclear cofactor p300 and its histone acetyl transferase activity and decreased expression and activity of histone deacetylases plays an important role in glucocorticoid-induced muscle proteolysis and wasting. Other mechanisms may also be involved in glucocorticoid-induced muscle wasting, including insulin resistance and store-operated calcium entry. Novel potential strategies to prevent or treat glucocorticoid-induced muscle wasting include the use of small molecule histone deacetylase activators, dissociated glucocorticoid receptor agonists, and 11 beta-hydroxysteroid dehydrogenase type 1 inhibitors. Summary An increased understanding of molecular mechanisms regulating glucocorticoid-induced muscle wasting will help develop new strategies to prevent and treat this debilitating condition.
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