Cardiac arrhythmia occurs frequently worldwide, and in severe cases can be fatal. Mitochondria are the power plants of cardiomyocytes. In recent studies, mitochondria under certain stimuli produced excessive reactive oxygen species (ROS), which affect the normal function of cardiomyocytes through ion channels and related proteins. Mitochondrial oxidative stress (MOS) plays a key role in diseases with multifactorial etiopathogenesis, such as arrhythmia; MOS can lead to arrhythmias such as atrial fibrillation and ventricular tachycardia. This review discusses the mechanisms of arrhythmias caused by MOS, particularly of ROS produced by mitochondria. MOS can cause arrhythmias by affecting the activities of Ca2+-related proteins, the mitochondrial permeability transition pore protein, connexin 43, hyperpolarization-activated cyclic nucleotide-gated potassium channel 4, and ion channels. Based on these mechanisms, we discuss possible new treatments for arrhythmia. Targeted treatments focusing on mitochondria may reduce the progression of arrhythmias, as well as the occurrence of severe arrhythmias, and may be effective for personalized disease prevention.
Keywords: Arrhythmia; Mitochondria; Molecular pathways; Preventive treatment; Reactive oxygen species; Targeted treatments.
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