Voltage-Gated Sodium Channels: A Therapeutic Target in Ischemic Heart Disease
Myocardial infarction (MI)-related arrhythmias are an essential risk factor in sudden cardiac death. Aberrant cardiac the cardiac voltage-gated sodium channel (Nav1.5) is important in the development of ventricular arrhythmias after an MI. These mechanisms are profoundly complex and involve sodium v...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
IMR Press
2025-06-01
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| Series: | Reviews in Cardiovascular Medicine |
| Subjects: | |
| Online Access: | https://www.imrpress.com/journal/RCM/26/6/10.31083/RCM27140 |
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| Summary: | Myocardial infarction (MI)-related arrhythmias are an essential risk factor in sudden cardiac death. Aberrant cardiac the cardiac voltage-gated sodium channel (Nav1.5) is important in the development of ventricular arrhythmias after an MI. These mechanisms are profoundly complex and involve sodium voltage-gated channel α subunit 5 (SCN5A) and sodium voltage-gated channel α subunit 10 (SCN10A) single nucleotide polymorphisms, aberrant splicing of SCN5A mRNAs, transcriptional and post-transcriptional regulation, translation, post-translational transport, and modification, along with protein degradation. These mechanisms ultimately promote a decrease in peak sodium currents, an increase in late sodium currents, and changes in sodium channel kinetics. This review aimed to explore the specific mechanisms of Nav1.5 in post-MI arrhythmias and summarize the potential of therapeutic drugs. An in-depth study of the effect of Nav1.5 on arrhythmias after myocardial ischemia is of crucial clinical significance. |
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| ISSN: | 1530-6550 |