Purpose of review
Striking sex differences exist not only in the incidence of cardiovascular disease, but also in the clinical outcomes. Although cardiovascular events occur earlier in men, in women, it appears they have poorer short-term and long-term outcomes following these events compared to men. Thus, intrinsic sex differences may exist not only in atherogenesis, but also with respect to cardiovascular adaptation/repair in response to ischemia and/or infarction. Angiogenesis, the growth of new blood vessels, is essential for organ development and is critical to cardiovascular repair/regeneration. Although the effect of estrogen on angiogenesis has been studied extensively, the role of androgens has remained largely unexplored.
Multiple lines of evidence now suggest an important role for androgens in cardiovascular repair and regeneration. Studies suggest that androgens stimulate angiogenesis via vascular endothelial growth factor-related mechanisms and by the stimulation of erythropoietin production. Furthermore, endothelial progenitor cells, important in angiogenesis, appear to be hormonally regulated and an important target of androgen action.
Given the age-related decline in androgens, the findings discussed here have implications for therapeutic angiogenesis and androgen replacement therapies in aging and hypogonadal men.