AKT1 and endothelial dysfunction: In particular, it has been reported that H2O2 generated reactive oxygen species (ROS) which subsequently activate the phosphorylation of AKT and ERK1/2 kinases in endothelial cells, and glucagon-like peptide-1 (GLP-1) attenuated ROS production accompanied with reducing AKT and ERK1/2 phosphorylation to reduce endothelial dysfunction and autophagy [36].