The molecular mechanisms underlying atrial fibrillation (AF), the most common form of arrhythmia, are poorly understood and therefore target-specific treatment options remain an unmet clinical need. Excitation–contraction coupling in cardiac myocytes requires high amounts of adenosine triphosphate (ATP), which is replenished by oxidative phosphorylation in mitochondria. Calcium (Ca²⁺) is a key regulator of mitochondrial function by stimulating the Krebs cycle, which produces nicotinamide adenine dinucleotide for ATP production at the electron transport chain and nicotinamide adenine dinucleotide phosphate for the elimination of reactive oxygen species (ROS). While it is now well established that mitochondrial dysfunction plays an important role in the pathophysiology of heart failure, this has been less investigated in atrial myocytes in AF. Considering the high prevalence of AF, investigating the role of mitochondria in this disease may guide the path towards new therapeutic targets. In this review, we discuss the importance of mitochondrial Ca²⁺ handling in regulating ATP production and mitochondrial ROS emission and how alterations, particularly in these aspects of mitochondrial activity, may play a role in AF. In addition to describing research advances, we highlight areas in which further studies are required to elucidate the role of mitochondria in AF.

心房颤动 (AF) 是最常见的心律失常形式，其分子机制知之甚少，因此靶向特异性治疗方案仍然是未满足的临床需求。心肌细胞中的兴奋-收缩耦合需要大量的三磷酸腺苷 (ATP)，而线粒体中的氧化磷酸化可以补充这些三磷酸腺苷 (ATP)。钙（Ca ²⁺) 是线粒体功能的关键调节剂，通过刺激三羧酸循环产生烟酰胺腺嘌呤二核苷酸用于电子传递链上的 ATP 生产和烟酰胺腺嘌呤二核苷酸磷酸盐用于消除活性氧 (ROS)。虽然现在已经确定线粒体功能障碍在心力衰竭的病理生理学中起着重要作用，但在 AF 心房肌细胞中的研究较少。考虑到 AF 的高患病率，研究线粒体在这种疾病中的作用可能会指导通往新治疗靶点的道路。在这篇综述中，我们讨论了线粒体 Ca ²⁺的重要性处理调节 ATP 产生和线粒体 ROS 释放以及如何改变，特别是在线粒体活性的这些方面，可能在 AF 中发挥作用。除了描述研究进展外，我们还强调了需要进一步研究以阐明线粒体在 AF 中的作用的领域。