Glucocorticoid Dysregulations and Their Clinical Correlates: From Receptors to Therapeutics

Marques, Andrea H.; Silverman, Marni N.; Sternberg, Esther M.

doi:10.1111/j.1749-6632.2009.04987.x

Cited by 158Stress Responses and CortisolAdrenal Hormones and DisordersEstrogen and related hormone effects

Glucocorticoid Dysregulations and Their Clinical Correlates: From Receptors to Therapeutics

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Marques, Andrea H., Silverman, Marni N., Sternberg, Esther M.·2009·Annals of the New York Academy of Sciences

DOI 10.1111/j.1749-6632.2009.04987.xPMC PMC2933142

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Abstract

Clinicians have long known that a substantial proportion of patients treated with high‐dose glucocorticoids experience a variety of serious side effects, including metabolic syndrome, bone loss, and mood shifts, such as depressive symptomatology, manic or hypomanic symptoms, and even suicide. The reason for individual variability in expression or severity of these side effects is not clear. However, recent emerging literature is beginning to shed light on possible mechanisms of these effects. As an introduction to this volume, this chapter will review the basic biology of glucocorticoid release and molecular mechanisms of glucocorticoid receptor function, and will discuss how dysregulation of glucocorticoid action at all levels could contribute to such side effects. At the molecular level, glucocorticoid receptor polymorphisms may be associated either with receptor hypofunction or hyperfunction and could thus contribute to differential individual sensitivity to the effects of glucocorticoid treatment. Numerous factors regulate hypothalamic‐pituitary‐adrenal (HPA) axis responsiveness, which could also contribute to individual differences in glucocorticoid side effects. One of these is sex hormone status and the influence of estrogen and progesterone on HPA axis function and mood. Another is immune system activity, in which immune molecules, such as interleukins and cytokines, activate the HPA axis and alter brain function, including memory, cognition, and mood. The effects of cytokines in inducing sickness behaviors, which overlap with depressive symptomatology, could also contribute to individual differences in such symptomatology. Taken together, this knowledge will have important relevance for identifying at‐risk patients to avoid or minimize such side effects when they are treated with glucocorticoids. A framework for assessment of patients is proposed that incorporates functional, physiological, and molecular biomarkers to identify subgroups of patients at risk for depressive symptomatology associated with glucocorticoid treatment, and for prevention of side effects, which in many cases can be life‐threatening.

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Aberrant glucocorticoid signaling is a mechanism that can influence the maintenance or progression of these disorders.
“Although the role that altered glucocorticoid sensitivity plays in the etiology of these disease conditions remains unclear, there is little doubt that aberrant glucocorticoid signaling is a mechanism that can influence the maintenance or progression of these disorders”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Marques et al., 2009
Hyperproduction of cortisol in Cushing's disease is responsible for the onset of depressive and manic symptoms and neurocognitive deficits, and directly influences the function and structure of various central nervous system areas.
“the hyperproduction of cortisol in Cushing's disease is responsible for the onset of depressive, manic symptoms and neurocognitive deficits, and directly influences the function and structure of various CNS areas (Sonino and Fava ,2001;Marques et al. 2009;Andela et al. 2015).”
From The HPA axis in bipolar disorder: Systematic review and meta-analysis (2016) · cites this paper as Marques et al. 2009
Prolonged hypercortisolemia can determine the onset of mood or psychotic symptoms.
“prolonged hypercortisolemia can determine the onset of mood or psychotic symptoms (Marques et al. 2009;Belvederi Murri et al. 2012)”
From The HPA axis in bipolar disorder: Systematic review and meta-analysis (2016) · cites this paper as Marques et al. 2009
Extensive evidence documents perturbed hypothalamic-pituitary-adrenal axis function as a result of early life stress and in depression and certain anxiety disorders, particularly PTSD.
“there is extensive evidence documenting perturbed HPA function both as a result of ELS and in the context of depression and certain anxiety disorders (particularly PTSD)”
From Gene–environment interactions: early life stress and risk for depressive and anxiety disorders (2011) · cites this paper as Marques et al. 2009

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From stress to inflammation and major depressive disorder: A social signal transduction theory of depression.
Slavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206 · see citing works
“T hi s ar tic le is in te nd ed so le ly fo r th e pe rs on al us e of th e in di vi du al us er an d is no t to be di ss em in at ed br oa dl y. Biddie, Conway-Campbell, & Lightman, 2012; Marques et al., 2009).”
Chronic stress, glucocorticoid receptor resistance, inflammation, and disease risk
Cohen, S., Janicki-Deverts, D., Doyle, W. J., Miller, G. E., Frank, E., Rabin, B. S., & Turner, R. B. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1118355109 · Cited by 1,419 · see citing works
The HPA axis in bipolar disorder: Systematic review and meta-analysis
Belvederi Murri, M., Prestia, D., Mondelli, V., Pariante, C., Patti, S., Olivieri, B., Arzani, C., Masotti, M., Respino, M., Antonioli, M., et al. (2016) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2015.10.014 · Cited by 391 · see citing works
Gene–environment interactions: early life stress and risk for depressive and anxiety disorders
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“Since altered sensitivity of GRs is thought to mediate HPA axis dysregulation in depression and PTSD (Raison and Miller 2003), genes regulating components of this system are likely candidates for GxE investigations of the etiopathology of depression and anxiety (Charney 2004; Wust et al. 2004a; Wust et al. 2004b).”
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Molecular links between endocrine, nervous and immune system during chronic stress
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Influence of chronic stress on brain corticosteroid receptors and HPA axis activity
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Testing the biological embedding hypothesis: Is early life adversity associated with a later proinflammatory phenotype?
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Stress-induced alterations in anxiety-like behavior and adaptations in plasticity in the bed nucleus of the stria terminalis
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Bone density and depressive disorder: a meta‐analysis
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Hypothalamic-pituitary-adrenal axis activity and cognition in major depression: The role of remission status
Salvat-Pujol, N., Labad, J., Urretavizcaya, M., de Arriba-Arnau, A., Segalàs, C., Real, E., Ferrer, A., Crespo, J. M., Jiménez-Murcia, S., Soriano-Mas, C., et al. (2017) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2016.11.007 · Cited by 47 · see citing works
Trajectories of relationship stress and inflammatory processes in adolescence
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Metabolic Syndrome and the Risk of Suicide: A Community-Based Integrated Screening Samples Cohort Study
Chang, J.-C., Yen, A. M.-F., Lee, C.-S., Chen, S. L.-S., Chiu, S. Y.-H., Fann, J. C.-Y., & Chen, H.-H. (2013) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000014 · Cited by 25 · see citing works
Serum/glucocorticoid regulated kinase 1 (SGK1) in neurological disorders: pain or gain
Howard, P. G., Zou, P., Zhang, Y., Huang, F., Tesic, V., Wu, C. Y.-C., & Lee, R. H.-C. (2024) · Experimental Neurology · doi:10.1016/j.expneurol.2024.114973 · Cited by 13 · see citing works
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Authors: Marques, A. H., Silverman, M. N., & Sternberg, E. M.
Affiliations: National Institutes of Health (US)
Corresponding author: Sternberg, Esther M.
Venue: Annals of the New York Academy of Sciences
Publisher: Wiley
Published: 2009-10
Volume: 1179
Issue: 1
Pages: 1-18
ISSN: 0077-8923 (ISSN-L)
1749-6632
DOI: 10.1111/j.1749-6632.2009.04987.x
PMC: PMC2933142
OpenAlex: W1976734955
Cited by: 158
References: 154
Citations by year: 2026: 7 · 2025: 4 · 2024: 7 · 2023: 9 · 2022: 5 · 2021: 6 · 2020: 8 · 2019: 11 · 2018: 7 · 2017: 12 · 2016: 8 · 2015: 7 · 2014: 14 · 2013: 10 · 2012: 16
FWCI: 0.75
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 33 d)
Locations: Annals of the New York Academy of Sciences (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Institute of Mental Health (ZIAMH002585)
Topics: Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Keywords: glucocorticoid adverse effects, glucocorticoid receptor, hypothalamic-pituitary-adrenal axis, HPA axis dysregulation, sex hormones, estrogen, progesterone, cytokines, sickness behavior, depression, mood disorders, suicide risk, metabolic syndrome, bone loss, interindividual variability, biomarkers, patient risk assessment, glucocorticoid therapy
MeSH terms: Animals, Cognition Disorders, Depressive Disorder, Forecasting, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Pituitary-Adrenal System, Receptors, Glucocorticoid, Gonadal Steroid Hormones

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Glucocorticoid Dysregulations and Their Clinical Correlates: From Receptors to Therapeutics

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