Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications
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 environm...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2025-08-01
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| Series: | Frontiers in Cardiovascular Medicine |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fcvm.2025.1506501/full |
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| author | Siyu Sun Zhanrui Zhang Yuxi Li Hui Zhang Huige Guo Guohui Chen Pei Wei Fei Lin Guoan Zhao |
| author_facet | Siyu Sun Zhanrui Zhang Yuxi Li Hui Zhang Huige Guo Guohui Chen Pei Wei Fei Lin Guoan Zhao |
| author_sort | Siyu Sun |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-bc03bf2faa1645b882d34261ac92069c |
| institution | DOAJ |
| issn | 2297-055X |
| language | English |
| publishDate | 2025-08-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Cardiovascular Medicine |
| spelling | doaj-art-bc03bf2faa1645b882d34261ac92069c2025-08-20T03:03:46ZengFrontiers Media S.A.Frontiers in Cardiovascular Medicine2297-055X2025-08-011210.3389/fcvm.2025.15065011506501Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implicationsSiyu SunZhanrui ZhangYuxi LiHui ZhangHuige GuoGuohui ChenPei WeiFei LinGuoan ZhaoVentricular 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.https://www.frontiersin.org/articles/10.3389/fcvm.2025.1506501/fullmyocardial infarctionventricular arrhythmiamitochondrialinflammationNa+/Ca2+ homeostasisfibrosis |
| spellingShingle | Siyu Sun Zhanrui Zhang Yuxi Li Hui Zhang Huige Guo Guohui Chen Pei Wei Fei Lin Guoan Zhao Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications Frontiers in Cardiovascular Medicine myocardial infarction ventricular arrhythmia mitochondrial inflammation Na+/Ca2+ homeostasis fibrosis |
| title | Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications |
| title_full | Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications |
| title_fullStr | Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications |
| title_full_unstemmed | Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications |
| title_short | Mitochondrial dysfunction as a central hub linking Na+/Ca2+ homeostasis and inflammation in ischemic arrhythmias: therapeutic implications |
| title_sort | mitochondrial dysfunction as a central hub linking na ca2 homeostasis and inflammation in ischemic arrhythmias therapeutic implications |
| topic | myocardial infarction ventricular arrhythmia mitochondrial inflammation Na+/Ca2+ homeostasis fibrosis |
| url | https://www.frontiersin.org/articles/10.3389/fcvm.2025.1506501/full |
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