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Glucocorticoid-induced apoptosis and cellular mechanisms of myopathy

Amie J Dirks-Naylor1, Carrie L Griffiths

  • 1Wingate University, School of Pharmacy, Wingate, NC 28174, United States. anaylor@wingate.edu

The Journal of Steroid Biochemistry and Molecular Biology
|June 13, 2009
PubMed

Insights

Glucocorticoid-induced myopathy, a side effect of steroid therapy, involves multiple cellular pathways. These mechanisms, including apoptosis and proteasome activity, contribute to muscle weakness.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Pharmacology

Background:

  • Glucocorticoid-induced myopathy is a frequent adverse effect of long-term glucocorticoid treatment.
  • Understanding the underlying molecular mechanisms is crucial for developing therapeutic strategies.

Purpose of the Study:

  • To review and synthesize the current understanding of the molecular mechanisms contributing to glucocorticoid-induced myopathy.
  • To highlight the various pathways implicated in glucocorticoid-induced muscle atrophy and apoptosis.

Main Methods:

  • Literature review of studies investigating glucocorticoid-induced myopathy.
  • Analysis of research on apoptotic signaling pathways (mitochondrial, Fas-mediated).
  • Examination of the roles of the proteasome, IGF-1 signaling, and ceramide.

Main Results:

  • Multiple mechanisms contribute to glucocorticoid-induced myopathy, including apoptosis and proteasome dysfunction.
  • Suppression of insulin-like growth factor 1 (IGF-1) signaling plays a role.
  • Ceramide accumulation is implicated in glucocorticoid-induced apoptosis and muscle damage.

Conclusions:

  • Glucocorticoid-induced myopathy results from a complex interplay of cellular mechanisms.
  • While the initiating event is unclear, mitochondrial-mediated apoptosis, Fas-mediated apoptosis, proteasome activity, IGF-1 suppression, and ceramide are all vital contributors.

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