Role of ferroptosis in the process of diabetes-induced endothelial dysfunction

Figure 6 Working model: activation of the p53-xCT (the substrate-specific subunit of system Xc^-)-glutathione axis and ferroptosis play a vital role in diabetes-induced endothelial dysfunction. In diabetes, p53 signaling is activated, and p53 can transcriptionally suppress xCT, in endothelial cells. The downregulation of xCT inhibits cystine uptake and reduces glutathione synthesis, which is involved in triggering ferroptosis in endothelial cells and ultimately leads to endothelial dysfunction. GSH: Glutathione; GSSG: Oxidized glutathione; GPX4: Glutathione peroxidase 4; ROS: Reactive oxygen species; ECs: Endothelial cells.