Increased late sodium currents are related to transcription of neuronal isoforms in a pressure-overload model

摘要

Aims The late and persistent sodium current (I_Na) has been identified as a target for anti-arrhythmia drugs in patients with heart failure (HF). However, the underlying mechanism of late I_Na (I_NaL) production remains uncertain. We hypothesized that transcriptional alteration among sodium channel (NaCh) isoforms may contribute to I_NaL in failing cardiomyocytes.