Inhibition of Na_V1.8 prevents atrial arrhythmogenesis in human and mice.

ABSTRACT: Pharmacologic approaches for the treatment of atrial arrhythmias are limited due to side effects and low efficacy. Thus, the identification of new antiarrhythmic targets is of clinical interest. Recent genome studies suggested an involvement of SCN10A sodium channels (Na_V1.8) in atrial electrophysiology. This study investigated the role and involvement of Na_V1.8 (SCN10A) in arrhythmia generation in the human atria and in mice lacking Na_V1.8. Na_V1.8 mRNA and protein were detected in human atrial myocardium at a significant higher level compared to ventricular myocardium. Expression of Na_V1.8 and Na_V1.5 did not differ between myocardium from patients with atrial fibrillation and sinus rhythm. To determine the electrophysiologi

SUBMITTER: Pabel S 

PROVIDER: S-EPMC7033079 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature