NFKB1 and endothelial dysfunction: In addition, treatments with PM, as well as JNK, p38 and NF-κB inhibitors, significantly blocked monocytes’ adhesion to endothelial monolayers against glycer-AGEs, suggesting that PM may be a pivotal regulator in the vascular inflammation that induces endothelial dysfunction via the MAPK/NF-κB pathways.