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Arteriosclerosis, Thrombosis, and Vascular Biology
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Published Online
on February 16, 2009

Arteriosclerosis, Thrombosis, and Vascular Biology. 2009
Published online before print February 16, 2009, doi: 10.1161/ATVBAHA.108.182279
A more recent version of this article appeared on March 1, 2009
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Submitted on December 8, 2008
Accepted on December 19, 2008

Estrogen and Mechanisms of Vascular Protection

Dongqi Xing ; Susan Nozell ; Yiu-Fai Chen ; Fadi Hage ; and Suzanne Oparil *

From the Vascular Biology and Hypertension Program, Division of Cardiovascular Disease, Department of Medicine (D.X., Y.-F.C., F.H., S.O.), and the Department of Cell Biology (S.N.), University of Alabama at Birmingham.

* To whom correspondence should be addressed. E-mail: soparil{at}uab.edu.

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-{kappa}B (NF{kappa}B) signaling pathway, as well as evidence that these protective mechanisms are lost in aging subjects.
Key words: estrogen • smooth muscle cells • inflammation • NF{kappa}B • vascular injury • oxidative stress


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