Mitochondrial fatty acid utilization increases chromatin oxidative stress in cardiomyocytes.

ABSTRACT: The inability of adult mammalian cardiomyocytes to proliferate underpins the development of heart failure following myocardial injury. Although the newborn mammalian heart can spontaneously regenerate for a short period of time after birth, this ability is lost within the first week after birth in mice, partly due to increased mitochondrial reactive oxygen species (ROS) production which results in oxidative DNA damage and activation of DNA damage response. This increase in ROS levels coincides with a postnatal switch from anaerobic glycolysis to fatty acid (FA) oxidation by cardiac mitochondria. However, to date, a direct link between mitochondrial substrate utilization and oxidative DNA damage is lacking. Here, we generated ROS-sensitive fluorescent sensors targeted to different subnuclea

SUBMITTER: Menendez-Montes I 

PROVIDER: S-EPMC8403954 | biostudies-literature | 2021 Aug

REPOSITORIES: biostudies-literature