Aging is one of the important risk factors for cardiovascular disease. Cardiovascular structure and function are continually under the remodeling process as we age. Two forms of vascular remodeling are associated with physiological and pathological processes: (1) angiogenesis, a process of developing new capillaries from pre-existing capillaries, and (2) arteriogenesis, a process of forming functional collateral conduit arteries from the existing small arteries or arterioles in the matured individual. Current research suggests that aging may attenuate the both angiogenesis and arteriogenesis by producing less angiogenic stimulating cytokines, or by increasing expression of anti-angiogenic factors. Yet, aged individuals remain responsive to physical (e.g. exercise training) and/or biochemical stimuli (e.g. exogenous angiogenic growth factors) to improve the angiogenic and arteriogenic capacity. At present our knowledge of the biological mechanisms of aging and angiogenesis/arteriogenesis interactions is limited. NO-donors, single (FGF-2, VEGF, PDGFs) or combined angiogenic growth factors (VEGF, Ang-1) demonstrated efficacy in promoting collateral function in the ischemic tissues of aged animals. Future studies should aim at the basis of aging-impaired angiogenic capacity at molecular level, and search for more effective strategies for therapeutic angiogenesis to treat ischemic cardiovascular diseases.