Reactive Oxygen Species Originating from Mitochondria Regulate the Cardiac Sodium Channel

Abstract

Background: Mutations in glycerol-3-phosphate dehydrogenase 1-like (GPD1-L) protein, a gene associated with Brugada Syndrome and Sudden Infant Death Syndrome, cause reduced cardiac sodium channel (Nav1.5) function by modulating NAD(H). NAD(H) regulates the cardiac Na+ channel through generation of reactive oxygen species (ROS). Here, we investigated the source of ROS induced by elevated NADH.