The place of estrogen in women's health remains controversial. Premenopausal women have a lower prevalence of cardiovascular disease (CVD) than menand hormone replacement therapy (HRT) decreases CVD in postmenopausal women. However, clinical trialsfailed to substantiate a protective effect of HRTand even showed some harm. Estrogen rapidly mediatesthe activation of endothelial nitric oxide synthase(eNOS) and increases production of nitric oxide(NO), an important factor for endothelial health.Distinctive results for eNOS, NO and superoxidelevels are highlighted by studies on acute and longterm effects of estrogen. In human endothelialcells, apoptosis induced by oxidized low-densitylipoprotein and the cytokine TNFα, associated withatherosclerosis, is reduced by estrogen. Estrogen's angiogenic properties help healthy endotheliumrespond to injury, but they also potentiate TNFα-induced angiogenesis, which revascularizes plaquesof women with advanced atherosclerosis andexacerbates cardiovascular events. Researchers and clinicians could appreciate this contribution to the undestanding of the paradoxical effects of estrogen on the vascular wall.
The place of estrogen in women's health remains controversial. Premenopausal women have a lower prevalence of cardiovascular disease (CVD) than menand hormone replacement therapy (HRT) decreases CVD in postmenopausal women. However, clinical trialsfailed to substantiate a protective effect of HRTand even showed some harm. Estrogen rapidly mediatesthe activation of endothelial nitric oxide synthase(eNOS) and increases production of nitric oxide(NO), an important factor for endothelial health.Distinctive results for eNOS, NO and superoxidelevels are highlighted by studies on acute and longterm effects of estrogen. In human endothelialcells, apoptosis induced by oxidized low-densitylipoprotein and the cytokine TNFα, associated withatherosclerosis, is reduced by estrogen. Estrogen's angiogenic properties help healthy endotheliumrespond to injury, but they also potentiate TNFα-induced angiogenesis, which revascularizes plaquesof women with advanced atherosclerosis andexacerbates cardiovascular events. Researchers and clinicians could appreciate this contribution to the undestanding of the paradoxical effects of estrogen on the vascular wall.
This volume presents the evolution of the authors' ideas about estrogen action and its modulation by a new group of drugs called SERMs (Selective Estrogen Receptor Modulators). The pioneering SERMs -...
Growing experimental evidence is beeing produced in support of the thesis that lipid pe,oxidation is an important mediator of both vascular and myocardial tissue derangement. Although the role of the...
An illuminating and timely synthesis of methodological and clinical studies showing how medical costs can be established, how the value of clinical outcomes can be assessed, and how difficult choices...
This contributed volume focuses on cardiovascular diseases (CVDs), and explores the ways in which signaling mechanisms at the biochemical, molecular, and cellular levels in the blood vessels...
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