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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.
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“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]
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Lee, S. R., Kim, H. K., Youm, J. B., Dizon, L. A., Song, I. S., Jeong, S. H., Seo, D. Y., Ko, K. S., Rhee, B. D., Kim, N., et al. (2012) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-012-1155-2 · Cited by 78
“in mitochondria [110] or cytoplasmic receptors [107] whose actions are unaffected by MR and GR [31, 40, 65].”
BackgroundDoyon, W. M., Thomas, A. M., Ostroumov, A., Dong, Y., & Dani, J. A. (2013) · Biochemical Pharmacology · doi:10.1016/j.bcp.2013.07.007 · Cited by 78
“ACTH stimulates the secretion of stress hormones, such as glucocorticoids, from the adrenal cortex [239], which influence neuronal activity via both genomic and non-genomic mechanisms [240].”
Dry eye syndrome: developments and lifitegrast in perspective
Lollett, I. V., & Galor, A. (2018) · Clinical ophthalmology · doi:10.2147/opth.s126668 · Cited by 81
“Treatment modalities: targeting inflammation Corticosteroids Mechanism of action Topical corticosteroids decrease inflammation primarily by binding to glucocorticoid receptors and regulating the expression of anti-inflammatory and proinflammatory genes.(110) Specifically, corticosteroids suppress NF-kB, a key transcri…”
Poulsen, R. C., Carr, A. J., & Hulley, P. A. (2011) · Endocrinology · doi:10.1210/en.2010-1087 · Cited by 77
Pacella, F., Romano, M. R., Turchetti, P., Tarquini, G., Carnovale, A., Mollicone, A., Mastromatteo, A., & Pacella, E. (2016) · International Journal of Ophthalmology · doi:10.18240/ijo.2016.10.10 · Cited by 77
Hussain, Y., & Khan, H. Z. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-818731-9.00068-9 · Cited by 90
Benefits and Risks of Dexamethasone in Noncardiac Surgery
Myles, P. S., & Corcoran, T. B. (2021) · Anesthesiology · doi:10.1097/aln.0000000000003898 · Cited by 79
Richardson, A. B., Bala, A., Wellman, S. S., Attarian, D. E., Bolognesi, M. P., & Grant, S. A. (2016) · The Journal of Arthroplasty · doi:10.1016/j.arth.2016.01.028 · Cited by 75
“43 The side effects of dexamethasone include increased risk of thromboembolism, peptic ulceration, 44 delayed wound healing, hyperglycemia and infection[21].”
BackgroundNew insights into the novel anti-inflammatory mode of action of glucocorticoids
Ingawale, D. K., & Mandlik, S. K. (2020) · Immunopharmacology and Immunotoxicology · doi:10.1080/08923973.2020.1728765 · Cited by 78
“The primary and secondary immune cells, tissues and organs were affected by the immunosuppressive, anti-inflammatory and anti-allergic effects of glucocorticoids via genomic and nongenomic mechanisms [28].”
BackgroundGenomic and non-genomic effects of glucocorticoids: implications for breast cancer.
Mitre-Aguilar, I. B., Cabrera-Quintero, A. J., & Zentella‐Dehesa, A. (2015) · Europe PMC (PubMed Central) · Cited by 74
Prenek, L., Boldizsár, F., Kugyelka, R., Ugor, E., Berta, G., Németh, P., & Berki, T. (2016) · APOPTOSIS · doi:10.1007/s10495-016-1320-8 · Cited by 79
“These latter involves non-nuclear actions like rapid eNOS (endothelial nitrogen oxide synthase) activation or alterations in signaling events and efector mechanisms of the cells [15], for example the interaction of the activated GR with cytoplasmic proteins like NF-κB (nuclear factor-kappaB) [16], or with molecules of…”
BackgroundRao, R., & Androulakis, I. P. (2019) · Hormones and Behavior · doi:10.1016/j.yhbeh.2019.02.018 · Cited by 81
Eagle, A. L., Knox, D., Roberts, M. M., Mulo, K., Liberzon, I., Galloway, M. P., & Perrine, S. A. (2012) · Neuroscience Research · doi:10.1016/j.neures.2012.11.001 · Cited by 75
Glucocorticoid therapy and ocular hypertension
Dibas, A., & Yorio, T. (2016) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2016.06.018 · Cited by 75
“Finally, GRα binds to a negative GRE (nGRE), resulting in transcription repression (Stahn and Buttgereit 2008; and Beck et al., 2009).”
BackgroundZhao, W., Qin, W., Pan, J., Wu, Y., Bauman, W. A., & Cardozo, C. P. (2008) · Biochemical and Biophysical Research Communications · doi:10.1016/j.bbrc.2008.11.123 · Cited by 71
Kasturi, S. P. T., & Sammaritano, L. R. (2015) · Rheumatic Disease Clinics of North America · doi:10.1016/j.rdc.2015.08.007 · Cited by 71
Gaber, T., Schellmann, S., Erekul, K. B., Fangradt, M., Tykwinska, K., Hahne, M., Maschmeyer, P., Wagegg, M., Stahn, C., Kolar, P., et al. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0903421 · Cited by 69
“Our understanding of the action of GCs has advanced in the last few years with regard to recent insights into signaling, regulation of transcription processes, and gene expression (genomic GC effects); dosage–plasma level– effect relationships; nongenomic GC effects; and new GC receptor (GCR) ligands (8, 9).”
BackgroundRapid Effects of Estradiol on Aggression in Birds and Mice: The Fast and the Furious: Fig. 1
Heimovics, S. A., Trainor, B. C., & Soma, K. K. (2015) · Integrative and Comparative Biology · doi:10.1093/icb/icv048 · Cited by 69
“Many of the rapid effects of glucocorticoids, especially on the immune system, also require high doses (Stahn and Buttgereit 2008).”
The Use of Glucocorticoids in Lupus Nephritis: New Pathways for an Old Drug
Mejia-Vilet, J. M., & Ayoub, I. M. (2021) · Frontiers in Medicine · doi:10.3389/fmed.2021.622225 · Cited by 74
“, interleukin-10, IκB, annexin A1), known as transactivation (8).”
BackgroundLuijten, R. K. M. A. C., Fritsch-Stork, R. D. E., Bijlsma, J. W. J., & Derksen, R. H. W. M. (2012) · Autoimmunity Reviews · doi:10.1016/j.autrev.2012.12.001 · Cited by 67
AMP-activated protein kinase confers protection against TNF-α-induced cardiac cell death
Kewalramani, G., Puthanveetil, P., Wang, F., Kim, M. S., Deppe, S., Abrahani, A., Luciani, D. S., Johnson, J. D., & Rodrigues, B. B. (2009) · Cardiovascular Research · doi:10.1093/cvr/cvp166 · Cited by 67
“Glucocorticoids such as DEX, which are potent anti-inflammatory drugs used for the treatment of a number of human diseases, are believed to act via both non-genomic (rapid) and genomic pathways.(41) In the present study, DEX treatment of cardiomyocytes led to an early (within 1 h) increase in AMPK phosphorylation that…”
BackgroundGlucocorticoid receptor signaling in the eye
Sulaiman, R. S., Kadmiel, M., & Cidlowski, J. A. (2017) · Steroids · doi:10.1016/j.steroids.2017.11.002 · Cited by 66
“Furthermore, GR 159 has been proposed to exert rapid non-genomic actions that do not require de novo 160 protein synthesis, by directly modulating signal transduction pathways [19].”
BackgroundWang, Z., Zhang, X., Cui, X., Cui, S., Yu, B., Sheng, Z., Li, S., Cao, Q., Huang, Y., Xu, Y.-P., et al. (2015) · Scientific Reports · doi:10.1038/srep09442 · Cited by 66
Dose- and time-dependent glucocorticoid receptor signaling in podocytes
Guess, A. J., Agrawal, S., Wei, C., Ransom, R. F., Benndorf, R., & Smoyer, W. E. (2010) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00161.2010 · Cited by 64
Mechanisms of glucocorticoid action and insensitivity in airways disease
Boardman, C., Chachi, L., Gavrila, A., Keenan, C. R., Perry, M. M., Xia, Y., Meurs, H., & Sharma, P. K. (2014) · Pulmonary Pharmacology & Therapeutics · doi:10.1016/j.pupt.2014.08.008 · Cited by 69
“negative GRE [50].”
BackgroundZanchi, N. E., Filho, M. A. D. S., Felitti, V., Nicastro, H., Lorenzeti, F. M., & Lancha, A. H. (2010) · Journal of Cellular Physiology · doi:10.1002/jcp.22141 · Cited by 62
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
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