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Related Experiment Videos

Glucocorticoids: exemplars of multi-tasking.

Julia C Buckingham1

  • 1Department of Cellular and Molecular Neuroscience, Division of Neuroscience and Mental Health, Imperial College London, Hammersmith W12 0NN. j.buckingham@imperial.ac.uk

British Journal of Pharmacology
|January 13, 2006
PubMed
Summary

Glucocorticoids are vital for treating inflammatory diseases and their dysregulation links to metabolic disorders. This review details advances in understanding glucocorticoid signaling, regulation, and their role in disease etiology.

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Area of Science:

  • Endocrinology
  • Molecular Pharmacology
  • Physiology

Background:

  • Adrenocortical extracts' clinical effects were noted over 80 years ago.
  • Glucocorticoids are crucial for treating inflammatory and autoimmune disorders.
  • Dysregulated glucocorticoid activity is linked to obesity, diabetes, metabolic syndrome, hypertension, and depression.

Purpose of the Study:

  • To review key advances in glucocorticoid physiology, pathology, and pharmacology.
  • To emphasize molecular mechanisms of glucocorticoid signaling.
  • To explore steroid access to target cell receptors and perinatal organizational effects.

Main Methods:

  • Review of existing literature on glucocorticoid research.
  • Focus on molecular mechanisms of glucocorticoid signaling pathways.

Related Experiment Videos

  • Analysis of regulatory mechanisms controlling steroid-receptor interactions.

    • Main Results:

    • Significant progress in understanding glucocorticoid signaling pathways.
    • Elucidation of complex mechanisms regulating steroid transport and receptor access.
    • Recognition of perinatal glucocorticoid actions and their long-term impact.

    Conclusions:

    • Glucocorticoids have diverse actions, with dysregulation contributing to major diseases.
    • Understanding molecular signaling and regulation is key to therapeutic development.
    • Perinatal exposure to glucocorticoids may have irreversible organizational effects relevant to disease etiology.