Chronic Inhibition of mROS Protects Against Coronary Endothelial Dysfunction in Mice With Diabetes

Abstract

Graphical AbstractChronic hyperglycemia during diabetes causes persistent overproduction of mitochondrial ROS (mROS), resulting in inhibition of endothelial SK channel activity, impairment of coronary endothelium-dependent relaxation and dysregulation of antioxidant/pro-cell death enzyme. Chronic inhibition of mROS with mito-Tempo prevents endothelial mROS production resulting in increasing endothelial SK currents, enhancing antioxidant enzyme production, and improving coronary endothelium-dependent relaxation.