Finerenone in Atrial Fibrillation: Molecular Mechanisms and Emerging Clinical Evidence

Abstract

Atrial fibrillation (AF) is a common tachyarrhythmia characterized by disorganized atrial electrical activity and ineffective contraction. It frequently coexists with various cardiovascular diseases and comorbidities, significantly increasing the risk of stroke, heart failure, and other adverse events. The overactivation of the renin-angiotensin-aldosterone system (RAAS), particularly the upregulation of the mineralocorticoid receptor (MR) signaling pathway, plays a central role in atrial remodeling and AF pathogenesis by driving myocardial inflammation and fibrosis. Finerenone, a novel non-steroidal, highly selective MR antagonist, exerts potent antifibrotic and anti-inflammatory effects by efficiently blocking MR. This review systematically elucidates the potential molecular mechanisms of finerenone in AF treatment and summarizes the emerging clinical evidence regarding its role in AF prevention and management, aiming to provide new insights for its application in the comprehensive management of AF.