The paper explores the intricate relationship between obesity, oxidative stress, inflammation, and mitochondrial dysfunction, and their role in the development and maintenance of atrial fibrillation (AF). Obesity is a significant risk factor for AF, with obese individuals having over two times the risk compared to non-obese individuals. The adipose tissue, a major endocrine organ, plays a crucial role in this relationship by inducing chronic inflammation, oxidative stress, and mitochondrial dysfunction. These processes contribute to structural and functional changes in cardiac myocytes, leading to AF. The paper discusses the complex interplay between these factors, highlighting how obesity-induced inflammation and oxidative stress can lead to atrial remodeling and increased susceptibility to AF. Additionally, it examines the impact of mitochondrial dysfunction on AF, including the production of reactive oxygen species (ROS) and the disruption of calcium handling, which further exacerbate the arrhythmia. The clinical implications of these mechanisms are also explored, emphasizing the potential of therapeutic strategies targeting inflammation, oxidative stress, and mitochondrial dysfunction to prevent and manage AF in obese patients. The paper concludes by suggesting that weight loss and interventions aimed at modulating these processes may be promising approaches to reduce the burden of AF in obese individuals.The paper explores the intricate relationship between obesity, oxidative stress, inflammation, and mitochondrial dysfunction, and their role in the development and maintenance of atrial fibrillation (AF). Obesity is a significant risk factor for AF, with obese individuals having over two times the risk compared to non-obese individuals. The adipose tissue, a major endocrine organ, plays a crucial role in this relationship by inducing chronic inflammation, oxidative stress, and mitochondrial dysfunction. These processes contribute to structural and functional changes in cardiac myocytes, leading to AF. The paper discusses the complex interplay between these factors, highlighting how obesity-induced inflammation and oxidative stress can lead to atrial remodeling and increased susceptibility to AF. Additionally, it examines the impact of mitochondrial dysfunction on AF, including the production of reactive oxygen species (ROS) and the disruption of calcium handling, which further exacerbate the arrhythmia. The clinical implications of these mechanisms are also explored, emphasizing the potential of therapeutic strategies targeting inflammation, oxidative stress, and mitochondrial dysfunction to prevent and manage AF in obese patients. The paper concludes by suggesting that weight loss and interventions aimed at modulating these processes may be promising approaches to reduce the burden of AF in obese individuals.