Abstract
Evidence exists that erectile dysfunction (ED) is analogous to endothelial dysfunction, a known precursor to atherosclerosis in terms of molecular mechanisms and underlying risk factors. These findings are discussed, along with the biologic underpinnings for the clinical observation that ED is an "early warning system" for atherosclerosis. Molecular mechanisms of ED as potential targets of novel therapies are considered, as well as the role of phosphodiesterase 5 inhibitors--currently the most effective treatment of ED--as promising therapies of cardiovascular diseases characterized by endothelial dysfunction.
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