Figure 1.

Simplified representation of the role of inflammatory molecules in atherogenesis. Injured endothelial cells (for example, by oxidised low density lipoprotein (LDL), cytokines, or lipopolysaccharide) produce cytokines (for example, interleukin (IL) 1), which stimulate the expression of adhesion proteins on the endothelial surface (for example, selectins and cell adhesion molecules). The latter recruit circulating leucocytes into the subendothelial space. Further cytokine release by infiltrated monocyte/macrophages (Mφ) and T lymphocytes promotes the formation of foam cells and the migration of smooth muscle cells from the media. The proinflammatory effects of IL 1 and tumour necrosis factor (TNF) are counterbalanced by the modulatory effects of transforming growth factor (TGF) produced by connective tissue cells. ICAM, intercellular adhesion molecule; VCAM, vascular cell adhesion molecule.