Mitochondria and the Pathophysiological Mechanism of Atrial Fibrillation

Abstract

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 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.

Blood Plasma Resistin and Atrial Fibrillation in Patients With Cardiovascular Disease

“…Many researchers have tried to associate the increased concentration of resistin in patients with CVD and left ventricular dysfunction and heart failure [16,18]. On the other hand, mitochondria play a central role in the function of cardiac myocyte and many of the pathophysiological processes involved in AF are related with the mitochondria function, including reactive oxygen species (ROS) formation and the changes in oxygen consumption in the myocardial cells of the heart [30][31][32][33][34]. Oxidative stress and inflammation are closely linked because inflammation can lead to ROS production and ROS could also promote the synthesis of pro-inflammatory cytokines such as interleukin (IL)-6, IL-8, IL-10, IL-12 and tumor necrosis factor alpha (TNF-α) [33].…”

Analysis of mitochondrial m1A/G RNA modification reveals links to nuclear genetic variants and associated disease processes

“…Furthermore, nuclear genetic variants (rs13874, rs1084535) associated with inferred methylation levels at multiple mt-tRNA P9 sites and at mt-RNR2 are in LD with rs34080181, which has been associated with atrial fibrillation 36 . High blood pressure is a risk factor for atrial fibrillation 37 , however, mitochondrial dysfunction itself has been implicated with the development of atrial fibrillation, through the generation of reactive oxidative species and the alteration of calcium homeostasis and oxygen consumption 38 .…”

Mitochondrial Pathobiology and Metabolic Remodeling in Progression to Overt Systolic Heart Failure

“…There is a growing line of advance that cardiac mitochondria are implicated in the pathogenesis of cardiac arrhythmias [77][78][79][80][81], beyond their role in the pathogenesis of HF and mitochondrial cardiomyopathies [82]. Moreover, skeletal muscle mitochondrial pathology is well recognized to play a fundamental role in the decline in functional capacity of HFpEF patient population and decreased peak oxygen consumption during exercise [83,84].…”