Interleukin-6: Molecular Mechanisms and Therapeutic Perspectives in Atrial Fibrillation
- PMID: 40035997
- DOI: 10.1007/s11596-025-00021-7
Interleukin-6: Molecular Mechanisms and Therapeutic Perspectives in Atrial Fibrillation
Abstract
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.
Conflict of interest statement
Declarations. Conflicts of Interest: The authors declare no conflicts of interest. Ethical Approval and Consent to Participate: This review relies solely on analysis of existing literature and does not include new experimental research; therefore, ethical approval and participant consent are not required. Human Ethics: This review relies solely on analysis of existing literature and does not include new experimental research; therefore, ethical approval and participant consent are not required. Consent for Publication: We collectively agree to submit this paper for publication in Current Medical Science and confirm that it has not been submitted to any other journal.
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