Pericellular and extracellular proteoglycans of the arterial intima interact with basic sequences of matrix proteins, lipoproteins, cytokines and enzymes. These associations appear to control the transit and function of the macromolecules in the intima. Alterations in these processes can cause focal deposition in the intima of modified apolipoprotein B-lipoproteins. Products of modified LDL appear to be atherogenic. In addition, imbalance in the function of cytokines that also interact with proteoglycans may contribute to the proliferative phase of atherogenesis and to the accumulation of foam cells.