NFKB1 and endothelial dysfunction: The binding of AGEs to RAGEs results in the downstream activation of NF-κB, leading to the upregulation of pro-inflammatory cytokines, adhesion molecules such as ICAM-1 and VCAM-1, and matrix metalloproteinases (MMPs), which contribute to endothelial dysfunction, monocyte recruitment, and plaque vulnerability [93].