From a mechanistic standpoint, these drugs recovered the diabetes-induced impairment of vasorelaxation; increased the serum NO levels and reductions of serum endothelin-1 and inflammatory cytokine levels such as VCAM-1, tumor necrosis factor (TNF)-α, and IL-6 levels; and inhibited the ROS production in the aorta [54], suggesting that incretin-based therapies improve diabetes-induced endothelial dysfunction by inhibiting inflammation and oxidative stress. Here, EDN1 is linked to diabetes mellitus.