The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Genomic and nongenomic effects of glucocorticoids
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.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“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 – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [76]
Citations
Cites
Primary structure and expression of a functional human glucocorticoid receptor cDNA
Hollenberg, S. M., Weinberger, C., Ong, E. S., Cerelli, G., Oro, A. E., Lebo, R. V., Thompson, E. B., Rosenfeld, M. G., & Evans, R. M. (1985) · Nature · doi:10.1038/318635a0 · Cited by 1,882
Mechanisms involved in the side effects of glucocorticoids
SCHACKE, H. (2002) · Pharmacology & Therapeutics · doi:10.1016/s0163-7258(02)00297-8 · Cited by 1,847
Oral corticosteroids and fracture risk: relationship to daily and cumulative doses
van Staa, T. P., Leufkens, H. G. M., Abenhaim, L., Zhang, B., & Cooper, C. C. (2000) · Lara D. Veeken · doi:10.1093/rheumatology/39.12.1383 · Cited by 699
Basic Guide to the Mechanisms of Antiestrogen Action
MacGregor, J. I., & Jordan, V. C. (1998) · Pharmacological Reviews · doi:10.1016/s0031-6997(24)01358-9 · Cited by 698
Steroid hormone receptors: an update
Beato, M. (2000) · Human Reproduction Update · doi:10.1093/humupd/6.3.225 · Cited by 615
Hafezi‐Moghadam, A., Simoncini, T., Yang, Z., Limbourg, F. P., Plumier, J.-C., Rebsamen, M. C., Hsieh, C.-M., Chui, D.-S., Thomas, K. L., Prorock, A. J., et al. (2002) · Nature Medicine · doi:10.1038/nm0502-473 · Cited by 596
Nissen, R. M., & Yamamoto, K. R. (2000) · Genes & Development · doi:10.1101/gad.827900 · Cited by 559
Buttgereit, F., Da Silva, J. A. P., Boers, M., Burmester, G.-R., Cutolo, M., Jacobs, J., Kirwan, J., Köhler, L., van Riel, P., Vischer, T., et al. (2002) · Annals of the Rheumatic Diseases · doi:10.1136/ard.61.8.718 · Cited by 544
da Silva, J. A. P., Jacobs, J. W. G., Kirwan, J., Boers, M., Saag, K. G., Inês, L. B. S., de Koning, E. J. P., Buttgereit, F., Cutolo, M., Capell, H., et al. (2005) · Annals of the Rheumatic Diseases · doi:10.1136/ard.2005.038638 · Cited by 529
A corticosteroid receptor in neuronal membranes
Orchinik, M., Murray, T. F., & Moore, F. L. (1991) · Science · doi:10.1126/science.2063198 · Cited by 523
Research works printed but not linked: 1
- Bijlsma JW et al. (2007) Systemic and intra-articular glucocorticoids in rheumatoid arthritis. In Rheumatoid arthritis, edn 2, 337–353 (Eds Firestein G. et al.) New York: Oxford University Press
Cited by
Sorted by citations
Neuroinflammation and depression: A review
Troubat, R., Barone, P., Leman, S., Desmidt, T., Cressant, A., Atanasova, B., Brizard, B., El Hage, W., Surget, A., Belzung, C., et al. (2021) · European Journal of Neuroscience · doi:10.1111/ejn.14720 · Cited by 1,107
“Once released, glucocorticoids can function in virtually all parts of the body and regulate a broad range of physiological processes through the genomic and non-genomic effects of glucocorticoid receptors (GRs) (Stahn & Buttgereit, 2008).”
BackgroundEULAR recommendations for the management of systemic lupus erythematosus: 2023 update
Fanouriakis, A., Kostopoulou, M., Andersen, J., Aringer, M., Arnaud, L., Bae, S., Boletis, J., Bruce, I. N., Cervera, R., Doria, A., et al. (2023) · Annals of the Rheumatic Diseases · doi:10.1136/ard-2023-224762 · Cited by 1,243
The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain
Bellavance, M.-A., & Rivest, S. (2014) · Frontiers in Immunology · doi:10.3389/fimmu.2014.00136 · Cited by 419
“, GPCRs, ion channels, TCR), and cytoplasmic proteins (MAPK and phospholipases) that indirectly impact on transcriptional activity (76, 79, 101).”
BackgroundLee, M., Pramyothin, P., Karastergiou, K., & Fried, S. K. (2013) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2013.05.029 · Cited by 399
“In addition, cytoplasmic or membrane bound GR causes rapid, nongenomic signaling [103], adding to the complexity of GC–GR mediated actions.”
BackgroundGlucocorticoid sensitivity in health and disease
Quax, R. A., Manenschijn, L., Koper, J. W., Hazes, J. M., Lamberts, S. W. J., van Rossum, E. F. C., & Feelders, R. A. (2013) · Nature Reviews Endocrinology · doi:10.1038/nrendo.2013.183 · Cited by 310
Metadata
- 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
- Published
- 2008-09-02
- Volume
- 4
- Issue
- 10
- Pages
- 525-533
- ISSN
- 1745-8382 (ISSN-L)
- 1745-8390
- 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 › Endocrinology › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
