In addition to causing direct cellular injury, ROS have the capacity to exacerbate inflammation and promote fibrosis by triggering various inflammatory signaling pathways such as nuclear factor kappa B (NF-κB), transforming growth factor beta (TGF-β), and the Nod-like receptor protein 3 (NLRP3) inflammasome, thereby driving AF progression (27). This evidence concerns the gene NLRP3 and atrial fibrillation.