Abstract
The voltage-gated sodium channel (NaV1.5) is critical for cardiac function. Rapid activation of NaV1.5 supports the initiation of the action potential, while ensuing inactivation is essential for proper repolarization. Human channelopathic mutations in NaV1.5 have been linked to various cardiac maladies, including cardiac arrhythmia, atrial fibrillation, and dilated cardiomyopathies. The carboxy-terminal domain (CTD) of NaV1.5 is critical for fine-tuning channel inactivation and is well-recognized as a hotspot for channelopathic mutations.
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