Phospho-ablation of cardiac sodium channel Na_v1.5 mitigates susceptibility to atrial fibrillation and improves glucose homeostasis under conditions of diet-induced obesity.

ABSTRACT:

Background

Atrial fibrillation (AF) is the most common sustained arrhythmia, with growing evidence identifying obesity as an important risk factor for the development of AF. Although defective atrial myocyte excitability due to stress-induced remodeling of ion channels is commonly observed in the setting of AF, little is known about the mechanistic link between obesity and AF. Recent studies have identified increased cardiac late sodium current (I_Na,L) downstream of calmodulin-dependent kinase II (CaMKII) activation as an important driver of AF susceptibility.

Methods

Here, we investigated a possible role for CaMKII-dependent I_Na,L in obesity-induced AF using wild-type (WT) and whole-body knock-in mice that ablates phosphorylation of the Na_v1

SUBMITTER: Dewal RS 

PROVIDER: S-EPMC8005377 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature