Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease

The mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. The mineralocorticoid receptor is also expressed in many tissues other than the kidney, such as adipose tissue, heart and vasculat...

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Main Authors: Stefania Gorini, Vincenzo Marzolla, Caterina Mammi, Andrea Armani, Massimiliano Caprio
Format: Article
Language:English
Published: MDPI AG 2018-09-01
Series:Biomolecules
Subjects:
Online Access:http://www.mdpi.com/2218-273X/8/3/96
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spelling doaj-9a875ed39a1941cab102ca3e1b308fd02020-11-25T00:16:18ZengMDPI AGBiomolecules2218-273X2018-09-01839610.3390/biom8030096biom8030096Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic DiseaseStefania Gorini0Vincenzo Marzolla1Caterina Mammi2Andrea Armani3Massimiliano Caprio4Laboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Rome, ItalyLaboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Rome, ItalyLaboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Rome, ItalyLaboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Rome, ItalyLaboratory of Cardiovascular Endocrinology, IRCCS San Raffaele Pisana, Via di Val Cannuta 247, 00166 Rome, ItalyThe mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. The mineralocorticoid receptor is also expressed in many tissues other than the kidney, such as adipose tissue, heart and vasculature. Recent studies have shown that MR plays a relevant role in the control of cardiovascular and metabolic function, as well as in adipogenesis. Dysregulation of aldosterone/MR signaling represents an important cause of disease as high plasma levels of aldosterone are associated with hypertension, obesity and increased cardiovascular risk. Aldosterone displays powerful vascular effects and acts as a potent pro-fibrotic agent in cardiovascular remodeling. Mineralocorticoid receptor activation regulates genes involved in vascular and cardiac fibrosis, calcification and inflammation. This review focuses on the role of novel potential biomarkers related to aldosterone/MR system that could help identify cardiovascular and metabolic detrimental conditions, as a result of altered MR activation. Specifically, we discuss: (1) how MR signaling regulates the number and function of different subpopulations of circulating and intra-tissue immune cells; (2) the role of aldosterone/MR system in mediating cardiometabolic diseases induced by obesity; and (3) the role of several MR downstream molecules as novel potential biomarkers of cardiometabolic diseases, end-organ damage and rehabilitation outcome.http://www.mdpi.com/2218-273X/8/3/96mineralocorticoid receptoraldosteronePBMCNGALGal-3PTGDSadipose tissue
collection DOAJ
language English
format Article
sources DOAJ
author Stefania Gorini
Vincenzo Marzolla
Caterina Mammi
Andrea Armani
Massimiliano Caprio
spellingShingle Stefania Gorini
Vincenzo Marzolla
Caterina Mammi
Andrea Armani
Massimiliano Caprio
Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
Biomolecules
mineralocorticoid receptor
aldosterone
PBMC
NGAL
Gal-3
PTGDS
adipose tissue
author_facet Stefania Gorini
Vincenzo Marzolla
Caterina Mammi
Andrea Armani
Massimiliano Caprio
author_sort Stefania Gorini
title Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
title_short Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
title_full Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
title_fullStr Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
title_full_unstemmed Mineralocorticoid Receptor and Aldosterone-Related Biomarkers of End-Organ Damage in Cardiometabolic Disease
title_sort mineralocorticoid receptor and aldosterone-related biomarkers of end-organ damage in cardiometabolic disease
publisher MDPI AG
series Biomolecules
issn 2218-273X
publishDate 2018-09-01
description The mineralocorticoid receptor (MR) was first identified as a blood pressure regulator, modulating renal sodium handling in response to its principal ligand aldosterone. The mineralocorticoid receptor is also expressed in many tissues other than the kidney, such as adipose tissue, heart and vasculature. Recent studies have shown that MR plays a relevant role in the control of cardiovascular and metabolic function, as well as in adipogenesis. Dysregulation of aldosterone/MR signaling represents an important cause of disease as high plasma levels of aldosterone are associated with hypertension, obesity and increased cardiovascular risk. Aldosterone displays powerful vascular effects and acts as a potent pro-fibrotic agent in cardiovascular remodeling. Mineralocorticoid receptor activation regulates genes involved in vascular and cardiac fibrosis, calcification and inflammation. This review focuses on the role of novel potential biomarkers related to aldosterone/MR system that could help identify cardiovascular and metabolic detrimental conditions, as a result of altered MR activation. Specifically, we discuss: (1) how MR signaling regulates the number and function of different subpopulations of circulating and intra-tissue immune cells; (2) the role of aldosterone/MR system in mediating cardiometabolic diseases induced by obesity; and (3) the role of several MR downstream molecules as novel potential biomarkers of cardiometabolic diseases, end-organ damage and rehabilitation outcome.
topic mineralocorticoid receptor
aldosterone
PBMC
NGAL
Gal-3
PTGDS
adipose tissue
url http://www.mdpi.com/2218-273X/8/3/96
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