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Voltage-Dependent Potassium Current Recording on H9c2 Cardiomyocytes via the Whole-Cell Patch-Clamp Technique
Published on: November 11, 2022
Voltage-Gated Sodium Channels: A Therapeutic Target in Ischemic Heart Disease
Xiao-Lu Zhang1, Tian-Peng Wei1, Fan Yang1
1Department of Cardiology, Wuxi People's Hospital Affiliated to Nanjing Medical University, 214023 Wuxi, Jiangsu, China.
Abstract:
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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