VCAM1 and endothelial dysfunction: Consistent with previous studies,18, 19 HG‐induced endothelial senescence promoted pronounced endothelial dysfunction as indicated by the down‐regulation of the eNOS protein level, the reduced bradykinin‐stimulated NO formation, the reduced NO‐mediated platelet anti‐aggregatory capability of ECs, and the up‐regulation of pro‐atherothrombotic markers including the cell adhesion molecule, VCAM‐1, and the physiological activator the coagulation cascade, tissue factor.