Document Detail


Glucocorticoid regulation of inflammation and its functional correlates: from HPA axis to glucocorticoid receptor dysfunction.
MedLine Citation:
PMID:  22823394     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Marni N Silverman; Esther M Sternberg
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Intramural; Review    
Journal Detail:
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:
Created Date:  2012-07-24     Completed Date:  2012-10-25     Revised Date:  2013-07-12    
Medline Journal Info:
Nlm Unique ID:  7506858     Medline TA:  Ann N Y Acad Sci     Country:  United States    
Other Details:
Languages:  eng     Pagination:  55-63     Citation Subset:  IM    
Copyright Information:
© 2012 New York Academy of Sciences. No claim to original U.S. Government works.
Affiliation:
Section on Neuroendocrine Immunology and Behavior, National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland, USA.
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MeSH Terms
Descriptor/Qualifier:
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
Grant Support
ID/Acronym/Agency:
ZIA MH002585-21/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Glucocorticoids; 0/Receptors, Glucocorticoid; 50-22-6/Corticosterone
Comments/Corrections

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