Genomic and nongenomic effects of glucocorticoids

Stahn, Cindy; Buttgereit, Frank

doi:10.1038/ncprheum0898

Cited by 594Estrogen and related hormone effectsAdrenal Hormones and DisordersReceptor Mechanisms and Signaling

Genomic and nongenomic effects of glucocorticoids

Stahn, Cindy, Buttgereit, Frank·2008·Nature Clinical Practice Rheumatology

DOI 10.1038/ncprheum0898

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Abstract

The strong anti-inflammatory and immunosuppressive effects of glucocorticoids are mediated primarily by the cytosolic glucocorticoid receptors. These receptors are members of the steroid hormone receptor family, a superfamily of ligand-inducible transcription factors, and exert genomic effects that can result in increased expression of regulatory-including anti-inflammatory-proteins (transactivation), or decreased production of proinflammatory proteins (transrepression). Transactivation is thought to be responsible for numerous adverse effects of glucocorticoids; transrepression is thought to be responsible for many of the clinically desirable anti-inflammatory and immunosuppressive effects of glucocorticoids. Optimized glucocorticoids, such as selective glucocorticoid receptor agonists, are being developed to try to minimize the adverse effects many patients experience. Glucocorticoids also exert their effects via rapid, nongenomic mechanisms that can be classified as involving nonspecific interactions of glucocorticoids with cellular membranes, nongenomic effects that are mediated by cytosolic glucocorticoid receptors, or specific interactions with membrane-bound glucocorticoid receptors. Increased understanding of these mechanisms of glucocorticoid action could enable the development of novel drugs with which to treat patients with inflammatory and autoimmune disease.

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GR-β permanently resides in the nucleus and acts as a dominant negative inhibitor of GR-α; its relative abundance, normally 1% of GR-α in the brain, is a key parameter dictating glucocorticoid responsiveness.
“In contrast, GR-β permanently resides in the nucleus where it selectively acts as a dominant negative inhibitor of GR-α (75). The relative abundance of the inhibitor GR-β, which normally represents only 1% of GR-α in the brain, is thus a key parameter in dictating GC responsiveness (76).”
From The HPA â€“ Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [76]

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Authors: Stahn, C., & Buttgereit, F.
Affiliations: Charité – Universitätsmedizin Berlin (DE)
Berlin Institute of Health at Charité - Universitätsmedizin Berlin (DE)
Corresponding author: Buttgereit, Frank
ORCID: Buttgereit, Frank
Venue: Nature Clinical Practice Rheumatology
Publisher: Springer Science and Business Media LLC
Published: 2008-09-02
Volume: 4
Issue: 10
Pages: 525-533
ISSN: 1745-8382 (ISSN-L)
1745-8390
DOI: 10.1038/ncprheum0898
OpenAlex: W1968436319
Cited by: 594
References: 65
Citations by year: 2026: 19 · 2025: 26 · 2024: 29 · 2023: 40 · 2022: 49 · 2021: 33 · 2020: 46 · 2019: 40 · 2018: 26 · 2017: 35 · 2016: 27 · 2015: 37 · 2014: 41 · 2013: 31 · 2012: 29
FWCI: 2.66
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Clinical Practice Rheumatology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords: glucocorticoids, glucocorticoid receptor, genomic mechanisms, transcriptional activation, transrepression, steroid hormone receptors, selective glucocorticoid receptor agonists, adverse effects, anti-inflammatory activity, immunosuppression, rheumatic diseases
MeSH terms: Anti-Inflammatory Agents, Cell Membrane, Dose-Response Relationship, Drug, Glucocorticoids, Humans, Immunosuppressive Agents, Ligands, Receptors, Glucocorticoid, Rheumatology, Transcriptional Activation, Genomics

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Genomic and nongenomic effects of glucocorticoids

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