Editorial

Drug Targeting of Estrogen Receptor Signaling in the Cardiovascular System: Preclinical and Clinical Studies

“…Abolished E2-dependent inhibition of the increase in medial area seen in wild-type mice (although did not prevent E2-dependent VSMC growth arrest) [127] Electric injury carotid artery ERαKOSt Abolished E2-dependent increase in reendothelization as compared to wild-type mice [121] Electric injury carotid artery ERβKOSt Increase in estradiol-dependent reendothelization similar to wild-type [121] Atherosclerosis ERαCHapoE double KO Abolished E2-dependent atheroprotective effects on lesion size and plasma cholesterol level [154] ERαKOCH: ERα-null mice generated in Chapel Hill [209]. These mice appear to have an incomplete disruption of ERα [124,125]. ERβKOCH: ERβ-null mice generated in Chapel Hill [210].…”

“…Disruption of either ERα [11] or ERβ [123] did not abolish E2-dependent inhibition of neointimal thickening in the mouse, suggesting that either of the two known ERs is sufficient for the vasoprotective function of E2, or that an ERα/ERβ-independent pathway is involved in these effects. It is important to note in this regard that the ERα-null mouse model used in these studies (ERα CH ) [11] appears to have an incomplete disruption of ERα [124,125]. Indeed, Pare et al have demonstrated the requirement of ERα for the protective effects of estrogen against vascular injury using a new ERα-null mouse model (ERα St ) [126].…”