A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification

Vascular calcification, which is common in the elderly and in patients with atherosclerosis, diabetes and chronic renal disease, increases the risk of cardiovascular morbidity and mortality. It is a complex, active and highly regulated cellular process that resembles physiological bone formation. It...

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Main Authors:	Zhu, Dongxing, Rashdan, Nabil A., Chapman, Karen E., Hadoke, Patrick WF, MacRae, Vicky E.
Format:	Online
Language:	English
Published:	Elsevier Science 2016
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5111541/

id	pubmed-5111541
recordtype	oai_dc
spelling	pubmed-51115412016-11-21 A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification Zhu, Dongxing Rashdan, Nabil A. Chapman, Karen E. Hadoke, Patrick WF MacRae, Vicky E. Article Vascular calcification, which is common in the elderly and in patients with atherosclerosis, diabetes and chronic renal disease, increases the risk of cardiovascular morbidity and mortality. It is a complex, active and highly regulated cellular process that resembles physiological bone formation. It has previously been established that pharmacological doses of glucocorticoids facilitate arterial calcification. However, the consequences for vascular calcification of endogenous glucocorticoid elevation have yet to be established. Glucocorticoids (cortisol, corticosterone) are released from the adrenal gland, but can also be generated within cells from 11-keto metabolites of glucocorticoids (cortisone, 11-dehydrocorticosterone [11-DHC]) by the enzyme, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). In the current study we hypothesized that endogenous glucocorticoids facilitate vascular smooth muscle cell (VSMC) calcification and investigated the receptor-mediated mechanism underpinning this process. Elsevier Science 2016-11 /pmc/articles/PMC5111541/ /pubmed/27153999 http://dx.doi.org/10.1016/j.vph.2016.04.005 Text en © 2016 The Authors http://creativecommons.org/licenses/by/4.0/ This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Zhu, Dongxing Rashdan, Nabil A. Chapman, Karen E. Hadoke, Patrick WF MacRae, Vicky E.
spellingShingle	Zhu, Dongxing Rashdan, Nabil A. Chapman, Karen E. Hadoke, Patrick WF MacRae, Vicky E. A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
author_facet	Zhu, Dongxing Rashdan, Nabil A. Chapman, Karen E. Hadoke, Patrick WF MacRae, Vicky E.
author_sort	Zhu, Dongxing
title	A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
title_short	A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
title_full	A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
title_fullStr	A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
title_full_unstemmed	A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
title_sort	novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification
description	Vascular calcification, which is common in the elderly and in patients with atherosclerosis, diabetes and chronic renal disease, increases the risk of cardiovascular morbidity and mortality. It is a complex, active and highly regulated cellular process that resembles physiological bone formation. It has previously been established that pharmacological doses of glucocorticoids facilitate arterial calcification. However, the consequences for vascular calcification of endogenous glucocorticoid elevation have yet to be established. Glucocorticoids (cortisol, corticosterone) are released from the adrenal gland, but can also be generated within cells from 11-keto metabolites of glucocorticoids (cortisone, 11-dehydrocorticosterone [11-DHC]) by the enzyme, 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1). In the current study we hypothesized that endogenous glucocorticoids facilitate vascular smooth muscle cell (VSMC) calcification and investigated the receptor-mediated mechanism underpinning this process.
publisher	Elsevier Science
publishDate	2016
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5111541/
_version_	1613729222179684352

A novel role for the mineralocorticoid receptor in glucocorticoid driven vascular calcification

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