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Université Paris Descartes, Sorbonne Paris Cité, Paris, France
Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Service de Génétique, Paris, France
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Université Paris Descartes, Sorbonne Paris Cité, Paris, France
Assistance Publique-Hôpitaux de Paris, Hôpital Européen Georges Pompidou, Service de Génétique, Paris, France
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Introduction Aldosterone and the mineralocorticoid receptor (MR) play a key role in the regulation of electrolyte balance and blood pressure. Abnormalities in aldosterone and MR function lead to salt-losing disorders or hypertension
Department of Medicine, Monash University, Clayton, Victoria, Australia
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effectively treated with mineralocorticoid receptor (MR) antagonists (MRAs). Targeted treatment of PA offers benefits above and beyond blood pressure control by mitigating the systemic effects of aldosterone-mediated MR activation ( Fig. 1 ). In this review
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Introduction The cloning of the mineralocorticoid receptor (MR) by Jeff Arriza working in the laboratory of Ron Evans ( Arriza et al . 1987 ) marked a critical inflexion point for research on aldosterone action. It followed the cloning of the
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Mineralocorticoid receptor signaling and cardiovascular disease While classically described as regulators of sodium and volume homeostasis in the kidney, aldosterone, and its receptor – the mineralocorticoid receptor (MR) – are increasingly
Endocrine Hypertension Group, Hudson Institute of Medical Research, Clayton, Australia
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Department of Medicine, Monash University, Clayton, Australia
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Department of Medicine, Monash University, Clayton, Australia
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Department of Medicine, Monash University, Clayton, Australia
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Introduction The purpose of this review is to explore whether the use of existing and novel biomarkers may have the potential to assist in the identification of patients with heart failure (HF) expected to respond to mineralocorticoid receptor
Paris Brain Institue-Institut du Cerveau, CNRS UMR7225, INSERM U1127, Hôpital de la Pitié Salpêtrière, Paris, France
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INSERM UMR 1195 (DHNS), Faculty of Medicine, Université Paris-Saclay, Le Kremlin-Bicêtre, France
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-Böhm et al. 2018 ). GC actions are mediated by two highly homologous members of the nuclear receptor superfamily, the mineralocorticoid receptor MR, coded by the Nr3c2 gene also named Mr ( Viengchareun et al. 2007 ) and the GC receptor GR ( Oakley
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have reported the importance of aldosterone and the mineralocorticoid receptor (MR) in CMS ( Zennaro et al. 2009 , Whaley-Connell et al. 2010 , Ronconi et al. 2012 , Even et al. 2014 ). Increasing evidence shows a link between obesity
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skeletal muscle mass ( Facchinello et al. 2017 , Faught & Vijayan 2019 a ). In teleosts, cortisol is the primary GC and the mode of action involves the activation of either GR and/or mineralocorticoid receptor (MR). Both these receptors are ligand
Department of Cardiology and Angiology I, Heart Center Freiburg University, Faculty of Medicine, University of Freiburg, Freiburg, Germany
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BIOSS Centre for Biological Signalling Studies, University of Freiburg, Freiburg, Germany
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Introduction Aldosterone mediates its effects via the mineralocorticoid receptor (MR), a ligand-activated transcription factor. Upon binding of aldosterone, MR interacts with a distinct DNA motif to regulate transcription of its target genes
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the mineralocorticoid receptor (MR) ( Reul & de Kloet 1985 , 1986 , Reul et al. 1987 ). Both MRs and GRs are highly expressed in the hippocampus, a key limbic area of the brain which is critically involved in regulating adaptive responses to