Atrial fibrillation (AF), the most common cardiac arrhythmia, is associated with substantial morbidity and mortality in patients with cardiovascular diseases (CVD). Accumulating evidence from preclinical models and clinical trials over the past decade indicates a robust link between excessive inflammatory activation and AF pathogenesis. The NACHT, LRR, and PYD domain-containing protein 3 (NLRP3) inflammasome plays a central role in this process. It can be activated by pathogen- and damage-associated molecular patterns (PAMPs/DAMPs). Upon recognition by pattern recognition receptors (PRRs), these signals trigger the nuclear factor κB (NF-κB) pathway, promoting transcriptional upregulation of NLRP3 . Subsequently, upstream signals such as potassium and chloride ion efflux induce NLRP3 inflammasome assembly and activation, mediating the maturation and secretion of proinflammatory cytokines including interleukin (IL)-1β and IL-18. Mechanistic studies, primarily conducted in rodent and canine models, show that NLRP3 inflammasome activation in cardiomyocytes and cardiac fibroblasts contributes to AF initiation and progression. These findings highlight the NLRP3 pathway as a promising therapeutic direction for AF. In this review, we summarize the regulatory mechanisms and biological roles of NLRP3 in AF and discuss NLRP3-targeted agents currently in clinical trials. Advancements in inflammasome-targeted therapies are expected to facilitate novel clinical interventions for AF and further clarify the role of NLRP3 in this arrhythmia.