Abstract: Atrial fibrillation (AF) is the most common arrhythmia in the elderly population. Studies have shown that the pathogenesis of AF is associated with aging, genetic mutations, inflammatory, oxidative stress, calcium disturbances and metabolic abnormalities. There is growing evidence that the above mechanisms play an important role in the evolution of atrial electrical remodeling, calcium handling and structural remodeling. In this review, we discuss the possible molecular mechanisms underlying the development of AF, which involve several typical inflammatory pathways and the potential of anti-inflammatory therapy, correction of metabolic abnormalities and other approaches in the prevention/treatment of AF.