| Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction. | |
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MedLine Citation:
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PMID: 22823394 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Enhanced susceptibility to inflammatory and autoimmune disease can be related to impairments in HPA axis activity and associated hypocortisolism, or to glucocorticoid resistance resulting from impairments in local factors affecting glucocorticoid availability and function, including the glucocorticoid receptor (GR). The enhanced inflammation and hypercortisolism that typically characterize stress-related illnesses, such as depression, metabolic syndrome, cardiovascular disease, or osteoporosis, may also be related to increased glucocorticoid resistance. This review focuses on impaired GR function as a molecular mechanism of glucocorticoid resistance. Both genetic and environmental factors can contribute to impaired GR function. The evidence that glucocorticoid resistance can be environmentally induced has important implications for management of stress-related inflammatory illnesses and underscores the importance of prevention and management of chronic stress. The simultaneous assessment of neural, endocrine, and immune biomarkers through various noninvasive methods will also be discussed. |
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Authors:
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Marni N Silverman; Esther M Sternberg |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Intramural; Review |
Journal Detail:
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Title: Annals of the New York Academy of Sciences Volume: 1261 ISSN: 1749-6632 ISO Abbreviation: Ann. N. Y. Acad. Sci. Publication Date: 2012 Jul |
Date Detail:
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Created Date: 2012-07-24 Completed Date: 2012-10-25 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 7506858 Medline TA: Ann N Y Acad Sci Country: United States |
Other Details:
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Languages: eng Pagination: 55-63 Citation Subset: IM |
Copyright Information:
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© 2012 New York Academy of Sciences. No claim to original U.S. Government works. |
Affiliation:
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Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Biological Markers Cardiovascular Diseases / metabolism, physiopathology Corticosterone / immunology, metabolism Cushing Syndrome / metabolism, physiopathology Depression / genetics, metabolism, physiopathology Glucocorticoids / immunology, metabolism* Humans Hypothalamo-Hypophyseal System / metabolism*, physiopathology Inflammation / genetics, metabolism*, physiopathology Metabolic Diseases / physiopathology Mice Neuroimmunomodulation / physiology Osteoporosis / metabolism, physiopathology Pituitary-Adrenal System / metabolism*, physiopathology Receptors, Glucocorticoid / genetics, immunology, metabolism* Stress, Psychological / genetics, metabolism, physiopathology |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Glucocorticoids; 0/Receptors, Glucocorticoid; 50-22-6/Corticosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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