Atrial fibrillation (AF) is a prevalent cardiac arrhythmia with a multifactorial pathophysiology involving electrical, structural, and autonomic remodeling of the atria. AF is closely associated with elevated interleukin-6 (IL-6) levels, which contribute to atrial remodeling and the progression of AF. This review summarizes the mechanisms by which IL-6 promotes AF through inflammatory pathways, atrial fibrosis, electrical remodeling, and calcium mishandling. Experimental models have demonstrated that IL-6 neutralization reduces the incidence of AF, highlighting its potential as a therapeutic target. Future studies should focus on IL-6 blockade strategies to manage AF, aiming to improve patient outcomes.
Keywords: Atrial fibrillation; Atrial remodeling; Inflammation; Interleukin-6; Therapeutic targets.
© 2025. The Author(s), under exclusive licence to Huazhong University of Science and Technology.