Fig. 7: Schematic diagram showing the cytoprotective signaling associated with MET in MGO-induced endothelial cell apoptosis.

The possible molecular mechanisms of MET in MGO-induced endothelial dysfunction in human ECs were explored. As depicted, MET inhibited the apoptotic signaling cascades initiated by MGO-generated ROS via modulating the PI3K/Akt and Nrf2/HO-1 signaling pathways. Furthermore, MET effectively exerts protective effects against MGO-induced oxidative stress, mitochondrial dysfunction, apoptosis, and inflammation in vitro and in vivo.