Atherosclerosis is clearly one of the most life-threatening diseases and a major cause of morbidity and mortality in industrialized countries. Typical arterial lesions contain both cells originating from the blood (monocytes/macrophages) and locally-recruited smooth muscle cells. The structure of the artery is profoundly disrupted. Degradation of arterial elastin fibers results in loss of elasticity, and several elastin peptides are released that can interact with various cells via an increasingly well-characterized elastin receptor. Elastin receptor-mediated reactions that are of obvious physiologic importance include vasodilating effects and induction of mesenchymal cell adhesion to elastin fibers. Other effects are potentially harmful, such as increased elastase production, free radical release, induction of LDL oxidation, and stimulation of endogenous cholesterol production. These deleterious effects become predominant during aging as a result of chronic exposure of the elastin receptor to circulating elastin peptides. This review describes the results of recent investigations into the biological effects of elastin peptides.