Ion channels are pore-forming transmembrane proteins involved with the transport of ions through cell membranes. In cardiac cells, the activity of these proteins is crucial for the excitation-contraction coupling process. Thus, ion channel malfunction represents one of the principal pathophysiological mechanisms underlying various inherited forms of arrhythmic disorders, so called channelopathies.
In cardiac cells, Nav1.5 channel represents the preponderant isoform of the voltage-gated sodium channels, and thereby plays an essential role in heart excitability. Nav1.5 dysfunction is linked with a broad range of inherited cardiac arrhythmias. Gain-of-function mutations of this channel are associated with many disorders such as the congenital long QT syndrome, atrial fibrillation, multifocal ectopic Purkinje-related premature contractions, and exercise-induced polymorphic ventricular tachycardia. The loss-of-function mutations are linked with Brugada syndrome, sick sinus syndrome, and cardiac conduction disease. In the same line, mutations in genes encoding Nav1.5 interacting proteins are also associated with many cardiac arrhythmias.
In this context, a better understanding of the pathophysiological mechanisms underlying sodium channelopathies-related arrhythmias may allow orient therapeutic decisions by targeting the biological effects of the disease-causing mutation, such as biophysical or folding defects.
In this Research Topic, we welcome colleagues to share their original research and review articles on the following subtopics related to the cardiac sodium channel Nav1.5:
1- Cardiac channelopathies
2- Pathophysiological mechanisms of Nav1.5 related arrhythmias.
3- Nav1.5 interacting proteins and its associated arrhythmias.
4- Pharmacology of the voltage-gated sodium channels in cardiac cells.
Ion channels are pore-forming transmembrane proteins involved with the transport of ions through cell membranes. In cardiac cells, the activity of these proteins is crucial for the excitation-contraction coupling process. Thus, ion channel malfunction represents one of the principal pathophysiological mechanisms underlying various inherited forms of arrhythmic disorders, so called channelopathies.
In cardiac cells, Nav1.5 channel represents the preponderant isoform of the voltage-gated sodium channels, and thereby plays an essential role in heart excitability. Nav1.5 dysfunction is linked with a broad range of inherited cardiac arrhythmias. Gain-of-function mutations of this channel are associated with many disorders such as the congenital long QT syndrome, atrial fibrillation, multifocal ectopic Purkinje-related premature contractions, and exercise-induced polymorphic ventricular tachycardia. The loss-of-function mutations are linked with Brugada syndrome, sick sinus syndrome, and cardiac conduction disease. In the same line, mutations in genes encoding Nav1.5 interacting proteins are also associated with many cardiac arrhythmias.
In this context, a better understanding of the pathophysiological mechanisms underlying sodium channelopathies-related arrhythmias may allow orient therapeutic decisions by targeting the biological effects of the disease-causing mutation, such as biophysical or folding defects.
In this Research Topic, we welcome colleagues to share their original research and review articles on the following subtopics related to the cardiac sodium channel Nav1.5:
1- Cardiac channelopathies
2- Pathophysiological mechanisms of Nav1.5 related arrhythmias.
3- Nav1.5 interacting proteins and its associated arrhythmias.
4- Pharmacology of the voltage-gated sodium channels in cardiac cells.
