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Special Issue "Role of Aldosterone Excess in Determining Cardiovascular Risk"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".

Deadline for manuscript submissions: 15 November 2021.

Special Issue Editor

Prof. Dr. Luigi Petramala
E-Mail Website
Guest Editor
Department of Translational and Precision Medicine, Unit of Secondary Arterial Hypertension, "Sapienza" University of Rome, Viale del Policlinico 155, 00165 Rome, Italy
Interests: Secondary hypertension; metabolic syndrome; adipose tissue

Special Issue Information

Dear Colleagues,

In recent years, numerous studies have confirmed the prominent role of primary hyperaldosteronism (PA), due to its high frequency among secondary forms of arterial hypertension and to specific deleterious effects on global cardiovascular risk; numerous studies have also evaluated how the excess of aldosterone directly causes important changes in the heart, vascular system, and metabolic balance, favoring arrhythmias, cardiac remodeling, metabolic alterations, increased oxidative stress, and thrombosis.

The purpose of this Special Issue is to highlight the direct role of excess aldosterone in the determination of higher global cardiovascular risk.

Prof. Dr. Luigi Petramala
Guest Editor

Manuscript Submission Information

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Keywords

  • primary hyperaldosteronism
  • global cardiovascular risk
  • heart
  • vascular system
  • metabolic alterations
  • oxidative stress
  • thrombosis

Published Papers (2 papers)

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Research

Article
Aldosterone Negatively Regulates Nrf2 Activity: An Additional Mechanism Contributing to Oxidative Stress and Vascular Dysfunction by Aldosterone
Int. J. Mol. Sci. 2021, 22(11), 6154; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22116154 - 07 Jun 2021
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Abstract
High levels of aldosterone (Aldo) trigger oxidative stress and vascular dysfunction independent of effects on blood pressure. We sought to determine whether Aldo disrupts Nrf2 signaling, the main transcriptional factor involved in antioxidant responses that aggravate cell injury. Thoracic aorta from male C57Bl/6J [...] Read more.
High levels of aldosterone (Aldo) trigger oxidative stress and vascular dysfunction independent of effects on blood pressure. We sought to determine whether Aldo disrupts Nrf2 signaling, the main transcriptional factor involved in antioxidant responses that aggravate cell injury. Thoracic aorta from male C57Bl/6J mice and cultured human endothelial cells (EA.hy926) were stimulated with Aldo (100 nM) in the presence of tiron [reactive oxygen species (ROS) scavenger, eplerenone [mineralocorticoid receptor (MR) antagonist], and L-sulforaphane (SFN; Nrf2 activator). Thoracic aortas were also isolated from mice infused with Aldo (600 μg/kg per day) for 14 days. Aldo decreased endothelium-dependent vasorelaxation and increased ROS generation, effects prevented by tiron and MR blockade. Pharmacological activation of Nrf2 with SFN abrogated Aldo-induced vascular dysfunction and ROS generation. In EA.hy926 cells, Aldo increased ROS generation, which was prevented by eplerenone, tiron, and SFN. At short times, Aldo-induced ROS generation was linked to increased Nrf2 activation. However, after three hours, Aldo decreased the nuclear accumulation of Nrf2. Increased Keap1 protein expression, but not activation of p38 MAPK, was linked to Aldo-induced reduced Nrf2 activity. Arteries from Aldo-infused mice also exhibited decreased nuclear Nrf2 and increased Keap1 expression. Our findings suggest that Aldo reduces vascular Nrf2 transcriptional activity by Keap1-dependent mechanisms, contributing to mineralocorticoid-induced vascular dysfunction. Full article
(This article belongs to the Special Issue Role of Aldosterone Excess in Determining Cardiovascular Risk)
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Article
Id2 Represses Aldosterone-Stimulated Cardiac T-Type Calcium Channels Expression
Int. J. Mol. Sci. 2021, 22(7), 3561; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073561 - 30 Mar 2021
Viewed by 702
Abstract
Aldosterone excess is a cardiovascular risk factor. Aldosterone can directly stimulate an electrical remodeling of cardiomyocytes leading to cardiac arrhythmia and hypertrophy. L-type and T-type voltage-gated calcium (Ca2+) channels expression are increased by aldosterone in cardiomyocytes. To further understand the regulation [...] Read more.
Aldosterone excess is a cardiovascular risk factor. Aldosterone can directly stimulate an electrical remodeling of cardiomyocytes leading to cardiac arrhythmia and hypertrophy. L-type and T-type voltage-gated calcium (Ca2+) channels expression are increased by aldosterone in cardiomyocytes. To further understand the regulation of these channels expression, we studied the role of a transcriptional repressor, the inhibitor of differentiation/DNA binding protein 2 (Id2). We found that aldosterone inhibited the expression of Id2 in neonatal rat cardiomyocytes and in the heart of adult mice. When Id2 was overexpressed in cardiomyocytes, we observed a reduction in the spontaneous action potentials rate and an arrest in aldosterone-stimulated rate increase. Accordingly, Id2 siRNA knockdown increased this rate. We also observed that CaV1.2 (L-type Ca2+ channel) or CaV3.1, and CaV3.2 (T-type Ca2+ channels) mRNA expression levels and Ca2+ currents were affected by Id2 presence. These observations were further corroborated in a heart specific Id2- transgenic mice. Taken together, our results suggest that Id2 functions as a transcriptional repressor for L- and T-type Ca2+ channels, particularly CaV3.1, in cardiomyocytes and its expression is controlled by aldosterone. We propose that Id2 might contributes to a protective mechanism in cardiomyocytes preventing the presence of channels associated with a pathological state. Full article
(This article belongs to the Special Issue Role of Aldosterone Excess in Determining Cardiovascular Risk)
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