The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.
Corticosteroid-insensitive asthma: molecular mechanisms
Abstract
Corticosteroids are the most potent anti-inflammatory agents used to treat chronic inflammatory diseases such as bronchial asthma. However, there are a small number (<5%) of asthmatic patients who do not respond well, or at all, to corticosteroid therapy - the corticosteroid-resistant and corticosteroid-dependent patients. Although this phenomenon is relatively uncommon, it poses a difficult therapeutic problem because few alternative therapies are available and these patients account for >50% of the health care costs of asthma. If the mechanisms for corticosteroid insensitivity are understood they may, in turn, provide insight into the key mechanism of corticosteroid action and allow a rational way to treat these individuals whose disease tends to be severe. Corticosteroid insensitivity is not limited to asthma and is a feature of other inflammatory diseases, such as rheumatoid arthritis and inflammatory bowel disease. Thus, elucidation of the cause for the relative lack of corticosteroid response in this subgroup of asthmatic individuals may have important implications for other diseases.
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Cites
AP-1 as a regulator of cell life and death
Shaulian, E., & Karin, M. (2002) · Nature Cell Biology · doi:10.1038/ncb0502-e131 · Cited by 2,961
DNA binding of the glucocorticoid receptor is not essential for survival
Reichardt, H. M., Kaestner, K. H., Tuckermann, J., Kretz, O., Wessely, O., Bock, R., Gass, P., Schmid, W., Herrlich, P., Angel, P., et al. (1998) · Cell · doi:10.1016/s0092-8674(00)81183-6 · Cited by 1,068
Antagonism of glucocorticoid receptor transcriptional activation by the c-Jun N-terminal kinase
Rogatsky, I., Logan, S. K., & Garabedian, M. J. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.5.2050 · Cited by 297
Discrimination between NL1- and NL2-Mediated Nuclear Localization of the Glucocorticoid Receptor
Savory, J. G. A., Hsu, B., Laquian, I. R., Giffin, W., Reich, T., Haché, R. J. G., & Lefebvre, Y. A. (1999) · Molecular and Cellular Biology · doi:10.1128/mcb.19.2.1025 · Cited by 222
Clinical aspects of glucocorticoid sensitivity
Lamberts, S. W. J., Huizenga, A. T. M., de Lange, P., de Jong, F. H., & Koper, J. W. (1996) · Steroids · doi:10.1016/0039-128x(96)00005-0 · Cited by 99
Cited by
Multifaceted mechanisms in COPD: inflammation, immunity, and tissue repair and destruction
Chung, K. F., & Adcock, I. M. (2008) · European Respiratory Journal · doi:10.1183/09031936.00018908 · Cited by 599
Self-citationGenomic and nongenomic effects of glucocorticoids
Stahn, C., & Buttgereit, F. (2008) · Nature Clinical Practice Rheumatology · doi:10.1038/ncprheum0898 · Cited by 594
Abraham, S. M., Lawrence, T., Kleiman, A., Warden, P., Medghalchi, M., Tuckermann, J., Saklatvala, J., & Clark, A. R. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20060336 · Cited by 430
“These patients can be diffi cult to treat eff ectively, but the molecular basis of GC insensitivity in infl ammatory disease remains poorly understood (2).”
BackgroundMolecular mechanisms of glucocorticoid action and selective glucocorticoid receptor agonists
Stahn, C., Löwenberg, M., Hommes, D. W., & Buttgereit, F. (2007) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2007.05.019 · Cited by 419
The mechanisms, diagnosis, and management of severe asthma in adults
Holgate, S. T., & Polosa, R. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69288-x · Cited by 398
Metadata
- Authors
- Adcock, I., & Lane, S.
- Venue
- Journal of Endocrinology
- Publisher
- Bioscientifica
- Published
- 2003-09-01
- Volume
- 178
- Issue
- 3
- Pages
- 347-355
- ISSN
- 0022-0795 (ISSN-L)
- 1479-6805
- OpenAlex
- W1976194871
- Cited by
- 179
- References
- 5
- FWCI
- 7.96
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
