Multiple aspects of mineralocorticoid selectivity
Abstract
Aldosterone regulates renal sodium reabsorption through binding to the mineralocorticoid receptor (MR). Because the glucocorticoid receptor (GR) is expressed together with the MR in aldosterone target cells, glucocorticoid hormones bound to GR may also intervene to modulate physiological functions in these cells. In addition, each steroid can bind both receptors, and the MR has equal affinity for aldosterone and glucocorticoid hormones. Several cellular and molecular mechanisms intervene to allow specific aldosterone regulatory effects, despite the large prevalence of glucocorticoid hormones in the plasma. They include the local metabolism of the glucocorticoid hormones into inactive derivatives by the enzyme 11beta-hydroxysteroid dehydrogenase; the intrinsic properties of the MR that discriminate between ligands through differential contacts; the possibility of forming homo- or heterodimers between MR and GR, leading to differential transactivation properties; and the interactions of MR and GR with other regulatory transcription factors. The relative contribution of each of these successive mechanisms may vary among aldosterone target cells (epithelial vs. nonepithelial) and according to the hormonal context. All these phenomena allow fine tuning of cellular functions depending on the degree of cooperation between corticosteroid hormones and other factors (hormonal or tissue specific). Such interactions may be altered in pathophysiological situations.
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In classic aldosterone target tissues, 11-beta hydroxysteroid dehydrogenase type 2 converts cortisol to cortisone, which has no mineralocorticoid receptor affinity, allowing aldosterone to specifically activate mineralocorticoid receptors.
“In classic aldosterone target tissues, such as the distal parts of the nephron and colon, the enzymatic breakdown of cortisol to cortisone by -beta hydroxysteroid dehydrogenase type (b-Hsd), which has no affinity for MRs, allowed for aldosterone to specifically bind to and activate MRs ().”
From Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management (2017) · cites this paper as [164]
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Lim-Tio, S. S., & Fuller, P. J. (1998) · Endocrinology · doi:10.1210/endo.139.4.5928 · Cited by 39 · see citing works
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Self-citationAlfaidy, N., Blot‐Chabaud, M., Bonvalet, J. P., & Farman, N. (1997) · Journal of Clinical Investigation · doi:10.1172/jci119785 · Cited by 37 · see citing works
Self-citationMultiple patterns of 11β-hydroxysteroid dehydrogenase catalytic activity along the mammalian nephron
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Mineralocorticoid and glucocorticoid receptor steroid binding and localization in colonic cells
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Autoradiographic determination of dexamethasone binding sites along the rabbit nephron
Farman, N., Vandewalle, A., & Bonvalet, J. P. (1983) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.1983.244.3.f325 · Cited by 30 · see citing works
Self-citationExpression of 11β-OHSD along the nephron of mammals and humans
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Detection of corticosteroid type I binding sites in heart
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Cellular mechanisms of action of mineralocorticoid hormones
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Molecular and cellular determinants of mineralocorticoid selectivity
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Self-citationInteractions of mineralocorticoids and glucocorticoids in epithelial target tissues
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Cysteines 849 and 942 of Human Mineralocorticoid Receptor Are Crucial for Steroid Binding
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Self-citationBAG-1M: A potential specificity determinant of corticosteroid receptor action
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Binding of aldosterone to cytoplasmic and nuclear receptors of the rabbit kidney
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Self-citationThe cardiac endocrine aldosterone system
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Glucocorticoid receptor signaling in health and disease
Kadmiel, M., & Cidlowski, J. A. (2013) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2013.07.003 · Cited by 849 · see citing works
Glucose Metabolism Abnormalities in Cushing Syndrome: From Molecular Basis to Clinical Management
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Quinkler, M., Meyer, B., Bumke-Vogt, C., Grossmann, C., Gruber, U., Oelkers, W., Diederich, S., & Bahr, V (2002) · European Journal of Endocrinology · doi:10.1530/eje.0.1460789 · Cited by 130 · see citing works
Sartorato, P., Lapeyraque, A.-L., Armanini, D., Kuhnle, U., Khaldi, Y., Salomon, R., Abadie, V., Di Battista, E., Naselli, A., Racine, A., et al. (2003) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2002-021932 · Cited by 85 · see citing works
- Authors
- Farman, N., & Rafestin-Oblin, M.-E.
- Affiliations
- Inserm (FR)
- ORCID
- Farman, Nicolette
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2001-02-01
- Volume
- 280
- Issue
- 2
- Pages
- F181-F192
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2182021623
- Cited by
- 268
- References
- 122
- Citations by year
- 2026: 6 · 2025: 3 · 2024: 5 · 2023: 12 · 2022: 8 · 2021: 9 · 2020: 5 · 2019: 8 · 2018: 8 · 2017: 10 · 2016: 11 · 2015: 12 · 2014: 8 · 2013: 16 · 2012: 13
- FWCI
- 1.94
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Renal Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hormonal Regulation and Hypertension
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
- Keywords
- mineralocorticoid receptor, glucocorticoid receptor, aldosterone, glucocorticoid metabolism, 11β-hydroxysteroid dehydrogenase, receptor heterodimerization, receptor transactivation, transcription factor interaction, renal sodium reabsorption
- MeSH terms
- Aldosterone, Animals, Glucocorticoids, Humans, Hydroxysteroid Dehydrogenases, Kidney, Mineralocorticoids, Receptors, Glucocorticoid, Receptors, Steroid, Receptors, Mineralocorticoid, 11-beta-Hydroxysteroid Dehydrogenases, 11-beta-Hydroxysteroid Dehydrogenase Type 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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