Abstract
Atrial fibrillation (AF), the most commonly diagnosed arrhythmia, affects a notable percentage of the population and constitutes a major risk factor for thromboembolic events and other heart-related conditions. Fibrosis plays an important role in the onset and perpetuation of AF through structural and electrical remodelling processes. Multiple molecular pathways are involved in atrial substrate modification and the subsequent maintenance of AF. In this review, we aim to recapitulate underlying molecular pathways leading to atrial fibrosis and to indicate existing gaps in the complex interplay of atrial fibrosis and AF.
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