Testosterone replacement attenuates intimal hyperplasia development in an androgen deficient model of vascular injury

AD increased IH development in response to vascular injury, whereas physiological TST replacement attenuated this effect. AD-induced IH occurs independent of matrix remodeling mechanisms known to be heavily involved in vascular dysfunction, and AD alone does not affect the UTS and/or UTSR mechanism. Exogenous TST and/or DHT increases UTSR pathway signaling in vitro and in vivo. This modulation correlates to a shift in cytoskeletal organization and may exacerbate vasoconstrictive pathogenesis. While physiological TST replacement attenuates AD-modulated IH development, its UTS-mediated effect on vasotone may prove deleterious to overall vascular function.