Sodium Channel Remodeling in Subcellular Microdomains of Murine Failing Cardiomyocytes.

ABSTRACT:

Background

Cardiac sodium channel (NaV1.5) dysfunction contributes to arrhythmogenesis during pathophysiological conditions. Nav1.5 localizes to distinct subcellular microdomains within the cardiomyocyte, where it associates with region-specific proteins, yielding complexes whose function is location specific. We herein investigated sodium channel remodeling within distinct cardiomyocyte microdomains during heart failure.

Methods and results

Mice were subjected to 6 weeks of transverse aortic constriction (TAC; n=32) to induce heart failure. Sham-operated on mice were used as controls (n=20). TAC led to reduced left ventricular ejection fraction, QRS prolongation, increased heart mass, and upregulation of prohypertrophic genes. Whole-cell sodium current (I_Na) dens

SUBMITTER: Rivaud MR 

PROVIDER: S-EPMC5779058 | biostudies-literature | 2017 Dec

REPOSITORIES: biostudies-literature