Mitochondrial ROS Drive Sudden Cardiac Death and Chronic Proteome Remodeling in Heart Failure.

ABSTRACT:

Rationale

Despite increasing prevalence and incidence of heart failure (HF), therapeutic options remain limited. In early stages of HF, sudden cardiac death (SCD) from ventricular arrhythmias claims many lives. Reactive oxygen species (ROS) have been implicated in both arrhythmias and contractile dysfunction. However, little is known about how ROS in specific subcellular compartments contribute to HF or SCD pathophysiology. The role of ROS in chronic proteome remodeling has not been explored.

Objective

We will test the hypothesis that elevated mitochondrial ROS (mROS) is a principal source of oxidative stress in HF and in vivo reduction of mROS mitigates SCD.

Methods and results

Using a unique guinea pig model of nonischemic HF that recapitulates important features of

SUBMITTER: Dey S 

PROVIDER: S-EPMC6057154 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature