Mineralocorticoid receptor activation and antagonism in cardiovascular disease: cellular and molecular mechanisms

IF 19.3 2区 医学 Q1 UROLOGY & NEPHROLOGY
Johann Bauersachs , Achim Lother
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引用次数: 14

Abstract

Aldosterone controls salt–water homeostasis by acting on the mineralocorticoid receptor (MR), a ligand-activated transcription factor, in kidney epithelial cells. However, it is now evident that the MR is expressed in multiple cell types and tissues, acting as a key driver of cardiovascular disease. MR antagonists have proven to be highly efficient in patients with heart failure and reduced ejection fraction, and they are a cornerstone of contemporary therapy. In the past decade, a series of experimental studies using models with cell type–specific MRs uncovered the cellular and molecular mechanisms underlying its detrimental effect on left ventricular remodeling. Based on these findings, the potential of MR antagonists has been evaluated in other cardiovascular diseases, including coronary artery disease, arterial hypertension, heart failure with preserved ejection fraction, pulmonary hypertension, atrial fibrillation, and heart valve disease. The present review summarizes the current knowledge on MR activation and antagonism in cardiovascular disease.

Abstract Image

心血管疾病中盐皮质激素受体的激活和拮抗作用:细胞和分子机制
醛固酮通过作用于肾上皮细胞中的盐皮质激素受体(MR)(一种配体激活的转录因子)来控制盐水稳态。然而,现在很明显,MR在多种细胞类型和组织中表达,是心血管疾病的关键驱动因素。MR拮抗剂已被证明对心力衰竭和射血分数降低的患者非常有效,是当代治疗的基石。在过去的十年里,一系列使用细胞类型特异性磁共振模型的实验研究揭示了其对左心室重构有害影响的细胞和分子机制。基于这些发现,已经评估了MR拮抗剂在其他心血管疾病中的潜力,包括冠状动脉疾病、动脉高压、射血分数保留的心力衰竭、肺动脉高压、心房颤动和心脏瓣膜疾病。本文综述了目前对MR在心血管疾病中的激活和拮抗作用的认识。
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来源期刊
Kidney International Supplements
Kidney International Supplements UROLOGY & NEPHROLOGY-
CiteScore
11.80
自引率
0.00%
发文量
13
期刊介绍: Kidney International Supplements is published on behalf of the International Society of Nephrology (ISN) and comes complimentary as part of a subscription to Kidney International. Kidney International Supplements is a peer-reviewed journal whose focus is sponsored, topical content of interest to the nephrology community.
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