Ion Channel and Structural Remodeling in Obesity-Mediated Atrial Fibrillation.

ABSTRACT:

Background

Epidemiological studies have established obesity as an independent risk factor for atrial fibrillation (AF), but the underlying pathophysiological mechanisms remain unclear. Reduced cardiac sodium channel expression is a known causal mechanism in AF. We hypothesized that obesity decreases Nav1.5 expression via enhanced oxidative stress, thus reducing I_Na, and enhancing susceptibility to AF.

Methods

To elucidate the underlying electrophysiological mechanisms a diet-induced obese mouse model was used. Weight, blood pressure, glucose, F₂-isoprostanes, NOX2 (NADPH oxidase 2), and PKC (protein kinase C) were measured in obese mice and compared with lean controls. Invasive electrophysiological, immunohistochemistry, Western blotting,

SUBMITTER: McCauley MD 

PROVIDER: S-EPMC7935016 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature