2007
DOI: 10.1002/ccd.21156
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Estrogen‐eluting stent implantation inhibits neointimal formation and extracellular signal‐regulated kinase activation

Abstract: Current study suggests that estrogen-eluting stents reduce neointimal formation and hence prevent restenosis after angioplasty possibly by inhibiting ERK activation in smooth muscle cells and promoting reendothelialization.

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Cited by 8 publications
(6 citation statements)
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“…Local delivery of estradiol decreases coronary angioplasty-induced neointimal hyperplasia in pigs (59, 60). These studies led to the development of estrogen-eluting stents, which reduce neointimal proliferation and induce reendothelialization in rabbit aorta (61) and porcine coronary artery (62). This protective effect of estrogen on vascular injury is evident in both ERα (63) and ERβ (63) knockout mice, indicating that another receptor may mediate this hormone's effects in the vasculature.…”
Section: Atherosclerosis and Vascular Remodelingmentioning
confidence: 99%
“…Local delivery of estradiol decreases coronary angioplasty-induced neointimal hyperplasia in pigs (59, 60). These studies led to the development of estrogen-eluting stents, which reduce neointimal proliferation and induce reendothelialization in rabbit aorta (61) and porcine coronary artery (62). This protective effect of estrogen on vascular injury is evident in both ERα (63) and ERβ (63) knockout mice, indicating that another receptor may mediate this hormone's effects in the vasculature.…”
Section: Atherosclerosis and Vascular Remodelingmentioning
confidence: 99%
“…It was the use of MPC polymer (PMPC) coatings on coronary stents to deliver antirestenosis therapies in the bloodstream that demonstrated the potential of PMPC materials in the field of drug delivery . In recent years, there have been reports of the use of water-soluble copolymers of MPC for solubilization of drugs such as paclitaxel and amphotericin B .…”
Section: Introductionmentioning
confidence: 99%
“…Other effects of estrogen in blood vessels include endothelial proliferation via activation of mitogen-activated protein kinase (MAPK); in contrast, MAPK in vascular smooth muscle (VSM) is suppressed [161,162]. The growth promoting effects of angiotensin II (AngII) on VSM is antagonized by estrogen, and it also suppresses VSM migration [163]. In rodent models, estrogen has been shown to enhance expression of angiogenic molecules like angiopoietin-1 and stimulate angiogenesis [164].…”
Section: Estrogen Endothelium and Vascular Smooth Musclementioning
confidence: 98%