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(Circulation Research. 2006;99:459.)
© 2006 American Heart Association, Inc.

Editorials

Estrogen and Different Aspects of Vascular Disease in Women and Men

Carl J. Pepine, Wilmer W. Nichols, Daniel F. Pauly

From the Division of Cardiovascular Medicine, University of Florida College of Medicine

Correspondence to Carl J. Pepine, MD, Division of Cardiovascular Medicine, University of Florida College of Medicine, 1600 SW Archer Road/Box 100277, Gainesville, FL 32610-0277. E-mail pepincj@medicine.ufl.edu

See related article, pages 477–484

Key Words: estrogen receptor-alpha (ESR1) • estrogen receptor-alpha genotype (ESR1) • gender-related vascular disease • women and vascular disease • men and vascular disease • vascular structure and function

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Considerable evidence indicates that sex hormones have an important influence on cardiovascular physiology and pathology.^1,2 Recent work suggests that a mechanism based on estrogen receptor-alpha (ESR1) contributes to a range of structural and functional responses that relate to vascular disease. Most of this work focuses on ESR1 activity within the endothelium and yields variable findings due, at least in part, to differences in the vascular bed or species studied, as well as other experimental conditions such as age, estrogen status, degree of preconstriction, etc. But many findings in conduit arteries (eg, more frequent plaque erosion, increased wall stiffness, spasm, etc) and microvessels (eg, reduced coronary flow reserve, hot flashes, etc) implicate smooth muscle cells (SMCs) in gender differences in vascular disease. These cells are directly responsible for extracellular matrix production and assure the integrity of the artery wall. They may be decreased, apoptotic, or dysfunctional in terms of synthesis and repair of extracellular matrix, which is destroyed in vulnerable plaque by macrophages.

In this issue of Circulation Research Montague and colleagues³ report that activation of ESR1 decreases human aorta SMC differentiation (Figure). Importantly, they found that SMCs of men, compared with women, had reduced ESR1 expression associated with increased differentiation markers. Their work suggests that ESR1 activation switches SMC to a form that may promote plaque vulnerability. Could different activational states of ESR1 be responsible for shifting the functional characteristics of SMCs toward a phenotype that explains some complexities of gender-related differences in vascular disease?

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Related Article:

Activation of Estrogen Receptor- Reduces Aortic Smooth Muscle Differentiation

Christine R. Montague, Melissa G. Hunter, Mikhail A. Gavrilin, Gary S. Phillips, Pascal J. Goldschmidt-Clermont, and Clay B. Marsh
Circ. Res. 2006 99: 477-484. [Abstract] [Full Text] [PDF]

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