Key result
Pharmacological inhibition or genetic ablation of NaV1.8 significantly reduced late Na+ current and proarrhythmic diastolic Ca2+ release, protecting against atrial fibrillation induction in mice.
Why the study?
Pharmacologic treatments for atrial arrhythmias have limited efficacy and side effects, making the identification of new antiarrhythmic targets of clinical interest.
Does pharmacological inhibition or genetic ablation of NaV1.8 prevent cellular arrhythmogenesis and atrial fibrillation induction in human atrial cardiomyocytes and murine models?
Population
Human atrial myocardium/cardiomyocytes and wild-type versus SCN10A-/- mice
Comparison
NaV1.8 inhibition or genetic ablation vs controls
Design
Translational basic science and animal study
Authors
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NaV1.8 inhibition may offer a selective AF target; leaves open efficacy in human atrial cardiomyocytes.
Does pharmacological inhibition or genetic ablation of NaV1.8 prevent cellular arrhythmogenesis and atrial fibrillation induction in human atrial cardiomyocytes and murine models?
Inhibition of NaV1.8 reduces late sodium current and proarrhythmic diastolic calcium release, presenting a novel selective therapeutic target for treating atrial arrhythmias.
Pabel et al. (2020) studied Atrial arrhythmias (n=54). NaV1.8 inhibition (A-803467 or PF-01247324) and genetic ablation vs. Control (vehicle) or Wild-type mice was evaluated on Late Na+ current (INaL) and atrial fibrillation inducibility. Pharmacological inhibition or genetic ablation of NaV1.8 significantly reduced late Na+ current and proarrhythmic diastolic Ca2+ release, protecting against atrial fibrillation induction in mice.
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