Glucocorticoid-induced apoptosis and cellular mechanisms of myopathy

• Published in: The Journal of steroid biochemistry and molecular biology Vol. 117; no. 1; pp. 1 - 7
• Main Authors: Dirks-Naylor, Amie J., Griffiths, Carrie L.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.10.2009
• Subjects: Animals; Apoptosis - drug effects; Atrophy; Cell death; Ceramides - metabolism; fas Receptor - metabolism; Glucocorticoids - adverse effects; Humans; Immunosuppressive Agents - adverse effects; Insulin-Like Growth Factor I - metabolism; Mitochondria; Mitochondria, Muscle - drug effects; Mitochondria, Muscle - metabolism; Models, Biological; Muscular Diseases - chemically induced; Muscular Diseases - metabolism; Muscular Diseases - pathology; Oxidative stress; Proteasome Endopeptidase Complex - metabolism; Signal Transduction - drug effects; Skeletal muscle; Atrophy; Oxidative stress; Mitochondria; Cell death; Skeletal muscle
• ISSN: 0960-0760; 1879-1220
• DOI: 10.1016/j.jsbmb.2009.05.014

Glucocorticoid-induced myopathy is a common side effect of chronic glucocorticoid therapy. Several mechanisms are currently being examined as ways in which glucocorticoid-induced myopathy occurs. These include apoptotic signaling through mitochondrial-mediated and Fas-mediated apoptosis, the role of the proteosome, the suppression of the IGF-1 signaling, and the role of ceramide in glucocorticoid-induced apoptosis and myopathy. It is difficult to differentiate which mechanism may be the initiating event responsible for the induction of apoptosis; however, all of the mechanisms play a vital role in glucocorticoid-induced myopathy.