cardiovascular disease is mainly dependent on direct actions on the vascular wall involving
activation of endothelial nitric oxide synthase (eNOS) via Akt and extracellular signal-
regulated protein kinase (ERK) cascades. Although raloxifene is also known to activate
eNOS in the vascular endothelium, the molecular mechanism responsible for this effect
remains to be elucidated. In studies of both human umbilical vein endothelial cells and …