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Aldosterone and the Mineralocorticoid Receptor in Atrial Fibrillation
Argen Mamazhakypov1,2, Remi Peyronnet3, Achim Lother1,4
1Institute of Experimental and Clinical Pharmacology and Toxicology (A.M., A.L.), Faculty of Medicine, University of Freiburg, Germany.
Hypertension (Dallas, Tex. : 1979)
|February 13, 2026
Summary
Aldosterone and mineralocorticoid receptor antagonists show promise in managing atrial fibrillation. These treatments may prevent and treat this common arrhythmia by targeting atrial remodeling and fibrosis.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Medicine
Background:
- Atrial fibrillation (AF) is a prevalent arrhythmia linked to stroke and heart failure.
- Pathophysiology involves atrial remodeling, increasing arrhythmia risk.
- Current treatments lack specific approaches targeting the proarrhythmic substrate.
Purpose of the Study:
- To review the role of aldosterone and mineralocorticoid receptor (MR) in atrial fibrillation pathogenesis.
- To summarize mechanistic evidence linking aldosterone to atrial remodeling and arrhythmia.
- To discuss the therapeutic potential of MR antagonists in AF prevention and treatment.
Main Methods:
- Review of clinical and experimental studies on aldosterone, MR, and atrial fibrillation.
- Analysis of mechanistic data on cellular processes modulated by MR activation.
- Synthesis of evidence on the efficacy of MR antagonists in various patient populations.
Main Results:
- Elevated aldosterone levels correlate with increased AF risk.
- MR antagonists reduce AF onset in diverse patient groups and may decrease recurrence in existing AF.
- Experimental studies confirm aldosterone's role in atrial inflammation, fibrosis, and arrhythmogenesis via MR activation.
Conclusions:
- Aldosterone and MR play a critical role in atrial fibrillation pathogenesis.
- MR activation drives atrial remodeling, inflammation, and fibrosis, contributing to AF.
- MR antagonists represent a promising therapeutic strategy for preventing and treating atrial fibrillation.
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