Obesity is a significant public health issue linked to various diseases, including atrial fibrillation (AF). This review explores the relationship between obesity, oxidative stress, inflammation, and mitochondrial dysfunction in the pathogenesis of AF. Obesity is associated with increased inflammation, oxidative stress, and mitochondrial dysfunction, which contribute to structural and functional changes in cardiac myocytes, promoting AF. The triad of inflammation, oxidative stress, and mitochondrial dysfunction plays a critical role in AF pathogenesis in obese individuals. Obesity-related changes in adipose tissue, such as chronic inflammation, oxidative stress, and insulin resistance, damage the atria and increase AF risk. Epicardial fat also contributes to AF through mechanical and paracrine mechanisms. Obesity affects cardiac structure and function, contributing to AF through the triad of inflammation, oxidative stress, and mitochondrial dysfunction. Inflammation increases AF susceptibility through electrical and structural remodeling. Obesity-induced inflammation leads to atrial myopathy, fibrosis, and electrical remodeling, promoting AF. Oxidative stress contributes to AF by altering calcium handling and increasing ROS production. Mitochondrial dysfunction in obesity leads to energy deficits and metabolic dysregulation, contributing to AF. Antioxidants and mitochondrial-targeted therapies may help reduce AF risk. Clinical implications include the need for targeted interventions to address inflammation, oxidative stress, and mitochondrial dysfunction in obese patients with AF. Further research is needed to develop effective therapies for AF in obese individuals.Obesity is a significant public health issue linked to various diseases, including atrial fibrillation (AF). This review explores the relationship between obesity, oxidative stress, inflammation, and mitochondrial dysfunction in the pathogenesis of AF. Obesity is associated with increased inflammation, oxidative stress, and mitochondrial dysfunction, which contribute to structural and functional changes in cardiac myocytes, promoting AF. The triad of inflammation, oxidative stress, and mitochondrial dysfunction plays a critical role in AF pathogenesis in obese individuals. Obesity-related changes in adipose tissue, such as chronic inflammation, oxidative stress, and insulin resistance, damage the atria and increase AF risk. Epicardial fat also contributes to AF through mechanical and paracrine mechanisms. Obesity affects cardiac structure and function, contributing to AF through the triad of inflammation, oxidative stress, and mitochondrial dysfunction. Inflammation increases AF susceptibility through electrical and structural remodeling. Obesity-induced inflammation leads to atrial myopathy, fibrosis, and electrical remodeling, promoting AF. Oxidative stress contributes to AF by altering calcium handling and increasing ROS production. Mitochondrial dysfunction in obesity leads to energy deficits and metabolic dysregulation, contributing to AF. Antioxidants and mitochondrial-targeted therapies may help reduce AF risk. Clinical implications include the need for targeted interventions to address inflammation, oxidative stress, and mitochondrial dysfunction in obese patients with AF. Further research is needed to develop effective therapies for AF in obese individuals.