Exercise restores dysregulated gene expression in a mouse model of arrhythmogenic cardiomyopathy.

ABSTRACT:

Aims

Arrhythmogenic cardiomyopathy (ACM) is a myocardial disease caused mainly by mutations in genes encoding desmosome proteins ACM patients present with ventricular arrhythmias, cardiac dysfunction, sudden cardiac death, and a subset with fibro-fatty infiltration of the right ventricle predominantly. Endurance exercise is thought to exacerbate cardiac dysfunction and arrhythmias in ACM. The objective was to determine the effects of treadmill exercise on cardiac phenotype, including myocyte gene expression in myocyte-specific desmoplakin (Dsp) haplo-insufficient (Myh6-Cre:DspW/F) mice.

Methods and results

Three months old sex-matched wild-type (WT) and Myh6-Cre:DspW/F mice with normal cardiac function, as assessed by echocardiography, were randomized to regular activity or

SUBMITTER: Cheedipudi SM 

PROVIDER: S-EPMC7177479 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature