Mitochondria and the Pathophysiological Mechanism of Atrial Fibrillation

Atrial fibrillation (AF) is the most common and significant cardiac arrhythmia in clinical practice, however the pathophysiological mechanism of AF has not been fully explained. At present, there are no available treatment options that can target the underlying pathophysiological processes of AF. Research on improving management strategies for AF can start with a further understanding of the changes of cells in AF. Mitochondria play central roles in the function of cardiac myocytes and many of the pathophysiological processes implicated in AF are relative to mitochondrial function, including formation of reactive oxygen species (ROS), calcium homeostasis, and alterations of oxygen consumption. The changes of levels of phosphocreatine, electron transfer chain proteins and differences in mitochondrial distribution further imply that mitochondria play a role in AF. Related studies of recent years are summarized, in order to elucidate the causal relationship between mitochondria and AF, and provide potential therapeutic target for the treatment and prevention of AF in clinical practice. In the article, we summarize the direct or indirect factors that affect mitochondria function and thus cause AF, including anticancer agents, surgery, gene, age, air pollution, oxidative stress, and β3-adrenoceptor (β3-AR). There is a close relationship between mitochondrial dysfunction and the occurrence of AF, which cannot be ignored, and further research in this area is needed.