Lipoprotein-matrix interactions play an important role in arterial disease. Extracellular matrix proteoglycans bind and retain specific positively charged domains on apolipoproteins B- and E-containing lipoproteins during atherogenesis. Retained lipoproteins can undergo several modifications, which may alter their interaction with extracellular matrix molecules. Growth factors, cytokines and oxidized low density lipoproteins influence proteoglycan structure, rendering them more likely to bind and retain lipoproteins during atherogenesis. Lipoproteins, native and modified, also can modulate the expression of several of the matrix degrading enzymes present in vascular tissue, thereby influencing plaque stability. Thus, the interaction of atherogenic lipoproteins with arterial wall matrix molecules can influence the genesis and progression of atherosclerosis and its complications.