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Estrogen and Mechanisms of Vascular Protection

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TLDR
Cellular/molecular mechanisms by which estrogen modulates injury-induced inflammation, growth factor expression, and oxidative stress in arteries and isolated vascular smooth muscle cells are reviewed, with emphasis on the role of estrogen receptors and the nuclear factor-kappaB (NFkappa B) signaling pathway.
Abstract
Estrogen has antiinflammatory and vasoprotective effects when administered to young women or experimental animals that appear to be converted to proinflammatory and vasotoxic effects in older subjects, particularly those that have been hormone free for long periods. Clinical studies have raised many important questions about the vascular effects of estrogen that cannot easily be answered in human subjects. Here we review cellular/molecular mechanisms by which estrogen modulates injury-induced inflammation, growth factor expression, and oxidative stress in arteries and isolated vascular smooth muscle cells, with emphasis on the role of estrogen receptors and the nuclear factor-κB (NFκB) signaling pathway, as well as evidence that these protective mechanisms are lost in aging subjects.

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Journal ArticleDOI

Estrogen and the cardiovascular system

TL;DR: Clinical investigations of estrogen have had mixed results, and not shown the clear-cut benefit of more basic investigations, so further basic research into the underlying molecular mechanisms of estrogen's actions is essential to provide a better comprehension of the many properties of this powerful hormone.
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Estrogen, hormonal replacement therapy and cardiovascular disease.

TL;DR: HRT has become one of the most controversial topics related to women's health and future studies are necessary if to understand the divergent published findings regarding HRT and develop new therapeutic strategies to improve the quality of life for women.
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Estrogenic endocrine disruptors: Molecular mechanisms of action.

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Women live longer than men even during severe famines and epidemics

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Low free testosterone predicts mortality from cardiovascular disease but not other causes: the Health in Men Study

TL;DR: Low testosterone predicts mortality from CVD but is not associated with death from other causes, and prevention of androgen deficiency might improve cardiovascular outcomes but is unlikely to affect longevity otherwise.
References
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Journal ArticleDOI

Inflammation, Atherosclerosis, and Coronary Artery Disease

TL;DR: The evidence is recounted that atherosclerosis, the main cause of CAD, is an inflammatory disease in which immune mechanisms interact with metabolic risk factors to initiate, propagate, and activate lesions in the arterial tree.
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Shared principles in NF-kappaB signaling

TL;DR: The authors synthesize some of the basic principles that have emerged from studies of NF-kappaB, and aim to generate a more unified view of the regulation of the transcription factor.
Journal ArticleDOI

Chemokines — Chemotactic Cytokines That Mediate Inflammation

TL;DR: This review introduces the burgeoning family of cytokines, with special emphasis on their role in the pathophysiology of disease and their potential as targets for therapy.
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A transmembrane intracellular estrogen receptor mediates rapid cell signaling.

TL;DR: It is found that of all G protein–coupled receptors characterized to date, GPR30 is uniquely localized to the endoplasmic reticulum, where it specifically binds estrogen and fluorescent estrogen derivatives.
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