Minireview: live and let die: molecular effects of glucocorticoids on bone cells

Lorenz C Hofbauer1, Martina Rauner

  • 1Division of Endocrinology, Diabetes, and Bone Diseases, Department of Medicine III, Technical University of Dresden, Fetscherstrasse 74, D-01307 Dresden, Germany. lorenz.hofbauer@uniklinikum-dresden.de

Insights

Glucocorticoids (GCs) treat immune diseases but cause osteoporosis. New GC receptor agonists offer targeted gene regulation, potentially reducing bone loss and improving therapies for bone conditions.

Area of Science:

  • Bone Biology
  • Endocrinology
  • Pharmacology

Background:

  • Glucocorticoids (GCs) are vital for treating immune-mediated diseases.
  • Long-term GC use leads to metabolic side effects, notably osteoporosis.
  • The glucocorticoid receptor (GC) mediates GC actions.

Purpose of the Study:

  • To review the cellular and molecular effects of GCs on bone cells.
  • To highlight signaling pathways for future therapeutic strategies.
  • To explore selective GC receptor modulators.

Main Methods:

  • Literature review of cellular and molecular mechanisms.
  • Analysis of glucocorticoid receptor signaling pathways.
  • Examination of GC effects on bone metabolism.

Main Results:

  • GCs exert complex effects on bone cells, influencing both formation and resorption.
  • GC receptor (GC) signaling pathways are key targets for modulating GC activity.
  • Selective GC receptor agonists show potential for dissociating therapeutic and adverse effects.

Conclusions:

  • Understanding GC actions on bone is crucial for mitigating side effects.
  • Targeting specific GC receptor pathways may lead to novel osteoporosis treatments.
  • Future strategies involve developing selective modulators to minimize bone loss.

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