January 10, 2026Reviews in Cardiovascular Medicine0 citationsOpen Access

Metabolic Remodeling and Mitochondrial Stress in Atrial Fibrillation: Mechanisms and Translational Targets

KGKonstantinos null GrigoriouNational and Kapodistrian University of Athens PKPaschalis null KarakasisAristotle University of Thessaloniki PTPanagiotis null TheofilisNational and Kapodistrian University of Athens

Key Result

Targeting metabolic alterations, particularly with SGLT2 inhibitors and GLP-1 receptor agonists, may help prevent the onset of atrial fibrillation.

Key Points

The central aim is to understand how metabolic remodeling and mitochondrial stress contribute to atrial fibrillation.
Comprehensive analysis of mechanisms linking metabolic changes and atrial fibrillation.
Evaluation of therapeutic strategies including SGLT2 inhibitors and GLP-1 receptor agonists.
Integration of multi-omics data for understanding metabolic diversity in atrial fibrillation.
Assessment of next-generation imaging for detecting pathologic substrates.
Atrial metabolic remodeling and mitochondrial stress facilitate the onset of atrial fibrillation.
Targeted therapies may restore metabolic homeostasis and mitigate arrhythmia effects.
Emerging approaches enhance the customization of treatments based on individual metabolic profiles.

Main Result

Absolute Event Rate: 0% vs 0%

Abstract

Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia and frequently co-occurs with metabolic diseases, such as diabetes and obesity. Due to the intricate and multifactorial pathophysiology of AF, this disorder often eludes effective prevention and durable control with current therapeutic strategies; thus, these strategies may not consistently mitigate the onset, persistence, and related adverse outcomes of AF. Moreover, atrial metabolic remodeling and mitochondrial stress can promote the development of atrial cardiomyopathy and AF through electrophysiological and structural changes. Hence, targeting these metabolic alterations may prevent the onset of this arrhythmia. A contemporary therapeutic paradigm prioritizes restoration of metabolic homeostasis, led by sodium–glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) receptor agonists and complemented by emerging mitochondria-targeted strategies with potential for incremental disease modification. Concurrently, integrative multi-omics is mapping atrial metabolic diversity in AF to support biomarker-guided, individualized interventions, while next-generation imaging is enhancing the detection of pathologic substrates and refining risk assessment. This review provides a comprehensive analysis of the mechanisms through which metabolic remodeling and mitochondrial stress cause AF, evaluates current experimental and diagnostic methods, and discusses emerging substrate-targeted therapies.

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