Figure 4  Role of macrophages in the pathogenesis of atherosclerosis. Disturbance of normal vascular physiology is characterized by endothelial activation which stimulates the expression of endothelial adhesion molecules (VCAM-1, ICAM-1) to favor the passage of inflammatory monocytes to the subendothelium. Modified LDL and other DAMPS are recognized by pattern-recognition receptors such as CD36 (scavenger receptor-B) in infiltrating macrophages. Thus, these innate cells are transformed into lipid-laden foam cells in the vasculature intima. The activation of NF-κB in response to ox-LDL induce the secretion of inflammatory cytokines (IL-1β, TNF), NO, MCP-1, and macrophage-derived matrix metalloproteinases (MMPs) that degrade the extracellular matrix generating a maladaptative inflammatory response and contribute to plaque formation.