Abstract
Relevance. Atrial fibrillation (AF) is the most common arrhythmia, which negatively affects the quality of life and significantly increases the risk of thrombosis, strokes and cardiovascular diseases. The pathogenesis of AF is a complex and multifactorial process in which inflammatory and immune mechanisms play an important role. In recent years, special attention has been paid to interleukins, cytokines that regulate the immune response, which may influence the development and maintenance of AF. The study of the role of interleukins in the pathogenesis of AF may provide new perspectives for understanding the mechanisms of the occurrence of this arrhythmia and the development of effective methods of its prevention and treatment. The study aimed to evaluate the influence of interleukins on the pathogenesis of atrial fibrillation and to identify possible mechanisms of their action. Methods. data concerning the role of interleukins in the pathogenesis of atrial fibrillation were analyzed during the analysis of scientific publications. A systematization of existing studies, including both clinical and experimental data that show a link between the levels of interleukins (IL-1, IL-6, IL-17 and others) and the development of AF was performed. Search methods included analyzing publications in PubMed, Scopus and Web of Science databases over the last ten years and using keywords related to interleukins and AF. Results. The results indicate that interleukins such as IL-1, IL-6, IL-17 and IL-18 play a significant role in the inflammatory processes associated with AF. Elevated levels of IL-6 correlate with worsening cardiac function and an increased likelihood of developing AF. In addition, IL-1 may contribute to myocardial remodeling, which is a key factor in the pathogenesis of AF. Other interleukins, such as IL-17, are also associated with inflammatory processes affecting cardiac electrical stability. Accumulating evidence suggests that interleukins can affect cellular hypertrophy and fibrosis, leading to changes in cardiac structure and contributing to the development of AF. The inclusion of interleukins in risk prediction models for the development of AF may improve preventive strategies and individualize the treatment of patients at risk. Conclusion. the analysis shows that interleukins play a key role in the pathogenesis of atrial fibrillation by participating in inflammatory processes and abnormalities in cardiac electrophysiology. Further studies are needed to clarify their mechanisms of action and to develop new therapeutic strategies aimed at reducing interleukin levels and improving the prognosis of patients with AF
Published Version
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