AffiliationDepartment of Molecular Medicine, Royal College of Surgeons in Ireland, Education, and Research Centre, Beaumont Hospital, Dublin 9, Ireland. firstname.lastname@example.org
MeSH11-beta-Hydroxysteroid Dehydrogenase Type 2
Cell Differentiation/drug effects
Cell Proliferation/drug effects
Cell Survival/drug effects
MAP Kinase Signaling System/physiology
Nephrons/drug effects/growth & development
Receptors, Mineralocorticoid/drug effects/*physiology
MetadataShow full item record
CitationFront Biosci. 2011 Jan 1;16:440-57.
JournalFrontiers in bioscience : a journal and virtual library
AbstractThe steroid hormone aldosterone is synthesized from cholesterol, mainly in the zona glomerulosa of the adrenal cortex. Aldosterone exerts its effects in the epithelial tissues of the kidney and colon and in non-epithelial tissues such as the brain and cardiovasculature. The genomic response to aldosterone involves dimerization of the mineralocorticoid receptor (MR), dissociation of heat shock proteins from MR, translocation of the aldosterone-MR complex to the nucleus and the concomitant regulation of gene expression. Rapid responses to aldosterone occur within seconds to minutes, do not involve transcription or translation and can modulate directly or indirectly the later genomic responses. Aside from the well-known effects of aldosterone on the regulation of sodium and water homeostasis, aldosterone can also produce deleterious structural changes in tissues by inducing hypertrophy and the dysregulation of proliferation and apoptosis, leading to fibrosis and tissue remodelling. Here we discuss the involvement of aldosterone-mediated rapid signalling cascades in the development of disease states such as chronic kidney disease and heart failure, and the antagonists that can inhibit these pathophysiological responses.
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