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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 In this special issue of JOE, we celebrate the thirtieth anniversary of cloning of the mineralocorticoid receptor (MR) in the Evans laboratory at the Salk Institute ( Arriza et al. 1987 ). This was an impressive achievement
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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
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
University of Groningen, University Medical Center, Groningen, The Netherlands
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Introduction On Tuesday April 14, 1987, while visiting Ron Evans and Jeff Arriza, we learned that they had cloned the mineralocorticoid receptor ( NR3C2 or MR). At the time, one of us (M Joëls) was working next door, with George Siggins and
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paper is part of a thematic review section on 30 Years of the Mineralocorticoid Receptor. The guest editors for this section were John Funder and Maria Christina Zennaro. References Alvarez de la Rosa D Gimenez I Forbush B Canessa
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Introduction The mineralocorticoid receptor (MR) was first cloned in 1987 ( Arriza et al. 1987 ) as a critical regulator of blood pressure through modulation of renal sodium handling in response to its ligand, the steroid hormone aldosterone
Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Monash Medical Centre, Clayton, Victoria, Australia
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Department of Molecular and Translational Research, Monash University, Melbourne, Victoria, Australia
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Introduction The mineralocorticoid receptor (MR) is an intracellular steroid hormone receptor, and a member of the nuclear receptor superfamily, that mediates the physiological action of two important adrenal steroids, aldosterone and cortisol
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Introduction The history of mineralocorticoid receptor antagonists (MRAs) was initially a history of ‘aldosterone antagonists (AAs)’ as the identification of the first AAs during the 1950s was driven by the goal of identifying inhibitors of
