REVIEW article
Front. Cardiovasc. Med.
Sec. Coronary Artery Disease
Volume 12 - 2025 | doi: 10.3389/fcvm.2025.1506501
This article is part of the Research TopicNovel Role and Mechanisms of Inflammation in Myocardial InfarctionView all 3 articles
Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications
Provisionally accepted
- The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
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Ventricular arrhythmia is the primary cause of sudden cardiac death in patients with myocardial infarction (MI). Myocardial inflammation and Na+/Ca2+ imbalance are the main triggering factors for life-threatening tachyarrhythmias after MI, which induce ion channel dysfunction, intracellular environment imbalance, tissue damage, and other alterations, subsequently resulting in modifications in cardiac conduction velocity and pathways. Subsequent adverse fibrotic remodeling provides a substrate for ventricular tachyarrhythmia (VT). Mitochondria, as the intersection site of these pathophysiological changes and the center of Na+/Ca2+ homeostasis and inflammatory crosstalk, may be key sites for the occurrence and development of ischemic arrhythmia. This review briefly outlines the roles of inflammation, Na+/Ca2+ homeostasis, and mitochondria in the damage, repair, and structural remodeling of infarcted hearts, in which these three are interconnected to provide a large number of substrates for VT.
Keywords: Myocardial Infarction, ventricular arrhythmia, mitochondrial, Inflammation, Na + /Ca 2+ homeostasis, Fibrosis
Received: 05 Oct 2024; Accepted: 29 Jul 2025.
Copyright: © 2025 Sun, Zhang, LI, Zhang, GUO, Chen, Wei, Lin and Guoan. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Fei Lin, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
Zhao Guoan, The First Affiliated Hospital of Xinxiang Medical University, Xinxiang, China
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