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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:995.)
© 2004 American Heart Association, Inc.

Editorials

Of Mice, Men, and Hormones

Virginia M. Miller; Donald J. Tindall; Peter Y. Liu

From the Departments of Surgery (V.M.M.), Physiology and Bioengineering (V.M.M.), Urology (D.J.T.), and Internal Medicine, Division of Endocrinology (P.Y.L.), Mayo Clinic College of Medicine, Rochester, MN.

Correspondence to Virginia M. Miller, MBA, PhD, Departments of Surgery and Physiology and Bioengineering, Mayo Clinic College of Medicine, Mayo Clinic, 200 First St. SW, Rochester, MN. E-mail miller.virginia@mayo.edu

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

Incidence of cardiovascular disease is consistently greater in men than in women during the first five decades of life.¹ Because this gender disparity begins early in life, it is likely that a combination of genetic, environmental (possibly intrauterine) factors, and actions of sex-specific hormones contribute to the disease process (see Nagel and vom Saal²). However, most research has focused on understanding how sex steroid hormones, estrogens and androgens, affect vascular function in men and women.

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Historically, an "estrogen protection" hypothesis, where estrogens limit development of atherosclerosis, has been tested, although an "androgen detrimental" hypothesis is also plausible, but less studied. Although these hypotheses provide a starting point for design of experiments to study effects of hormones on vascular function, review of available data suggests a more complex interaction among the sex steroids than this simple dichotomy.³ Therefore, new approaches are needed to dissect mechanisms of how sex steroids interact in development of vascular disease in both sexes.

The study by Villablanca et al, reported in this issue, uses an approach of examining the contribution of estrogen receptor alpha (ESR1) in development of early atheroma in male mice.⁴ The design is based on two published lines of research: one which forms the basis of the estrogen "protection" hypothesis, and the other which suggests that disruption and/or polymorphisms in ESR1 are associated with accelerated atherosclerosis and cardiovascular events in men.

The estrogen protection hypothesis arose predominately from large cohort studies, where perimenopausal women treated with estrogen or estrogen-progestin . . . [Full Text of this Article]

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