Mitochondrial Dysfunction in Cardiac Arrhythmias

Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are an organelle generating ATP, thereby satisfying the energy demand of the incessant electrical activity in the heart. In arrhythmias, the homeostatic supply-demand...

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Bibliographic Details
Published in:Cells (Basel, Switzerland) Switzerland), 2023-02, Vol.12 (5), p.679
Main Authors: Deng, Jielin, Jiang, Yunqiu, Chen, Zhen Bouman, Rhee, June-Wha, Deng, Yingfeng, Wang, Zhao V
Format: Article
Language:English
Subjects:
Adenosine Triphosphate
Analysis
Arrhythmia
Arrhythmias, Cardiac - pathology
ATP supply
Cardiac arrhythmia
Cardiomyocytes
Care and treatment
Complications and side effects
Diagnosis
Electrical stimuli
Electrophysiology
Excitability
Fatty acids
Gap junctions
Glucose
Health aspects
Heart
Homeostasis
Humans
Inflammation
Intestinal microflora
Microbiomes
Mitochondria
Mitochondria - pathology
Mitochondrial diseases
mitochondrial dysfunction
Molecular modelling
Pathophysiology
Potassium
Quality of life
Reactive Oxygen Species
Reperfusion
Review
Risk factors
Tachyarrhythmia
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Summary:Electrophysiological and structural disruptions in cardiac arrhythmias are closely related to mitochondrial dysfunction. Mitochondria are an organelle generating ATP, thereby satisfying the energy demand of the incessant electrical activity in the heart. In arrhythmias, the homeostatic supply-demand relationship is impaired, which is often accompanied by progressive mitochondrial dysfunction leading to reduced ATP production and elevated reactive oxidative species generation. Furthermore, ion homeostasis, membrane excitability, and cardiac structure can be disrupted through pathological changes in gap junctions and inflammatory signaling, which results in impaired cardiac electrical homeostasis. Herein, we review the electrical and molecular mechanisms of cardiac arrhythmias, with a particular focus on mitochondrial dysfunction in ionic regulation and gap junction action. We provide an update on inherited and acquired mitochondrial dysfunction to explore the pathophysiology of different types of arrhythmias. In addition, we highlight the role of mitochondria in bradyarrhythmia, including sinus node dysfunction and atrioventricular node dysfunction. Finally, we discuss how confounding factors, such as aging, gut microbiome, cardiac reperfusion injury, and electrical stimulation, modulate mitochondrial function and cause tachyarrhythmia.
ISSN:2073-4409
2073-4409
DOI:10.3390/cells12050679