Key result
Nav1.5 cardiac sodium channels are modulated by various factors and their alterations are associated with pathogenic conditions such as Long QT syndrome, Brugada syndrome, and atrial fibrillation.
Nav1.5 cardiac sodium channels are complexly regulated and their dysfunction is fundamentally linked to the pathogenesis of various congenital and acquired cardiac arrhythmias.
Nav1.5 dysfunction warrants arrhythmia evaluation; confirms pathogenic links but leaves targeted therapies open.
Voltage-gated sodium channels constitute a group of membrane proteins widely distributed thought the body. In the heart, there are at least six different isoforms, being the Nav1.5 the most abundant. The channel is composed of an α subunit that is formed by four domains of six segments each, and four much smaller β subunits that provide stability and integrate other channels into the α subunit. The function of the Nav1.5 channel is modulated by intracellular cytoskeleton proteins, extracellular proteins, calcium concentration, free radicals, and medications, among other things. The study of the channel and its alterations has grown thanks to its association with pathogenic conditions such as Long QT syndrome, Brugada syndrome, atrial fibrillation, arrhythmogenic ventricular dysplasia and complications during ischemic processes.
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Ariza et al. (2015) conducted a review in Cardiac sodium channel alterations. Nav1.5 cardiac sodium channels was evaluated. Nav1.5 cardiac sodium channels are modulated by various factors and their alterations are associated with pathogenic conditions such as Long QT syndrome, Brugada syndrome, and atrial fibrillation.
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