Hyperhomocysteinemia is a risk factor for cardiovascular disease, stroke, and thrombosis. Several animal models of hyperhomocysteinemia have been developed by using both dietary and genetic approaches. These animal models have provided considerable insight into the mechanisms underlying the adverse vascular effects of hyperhomocysteinemia. Accumulating evidence suggests a significant role of altered cellular redox reactions in the vascular phenotype of hyperhomocysteinemia. Redox effects of hyperhomocysteinemia are particularly important in mediating the adverse effects of hyperhomocysteinemia on the endothelium, leading to loss of endothelium-derived nitric oxide and vasomotor dysfunction. Redox reactions also may be key factors in the development of vascular hypertrophy, thrombosis, and atherosclerosis in hyperhomocysteinemic animals. In this review, we summarize the metabolic relations between homocysteine and the cellular redox state, the vascular phenotypes that have been observed in hyperhomocysteinemic animals, the evidence for altered redox reactions in vascular tissue, and the specific redox reactions that may mediate the vascular effects of hyperhomocysteinemia.