Horm Metab Res 2013; 45(10): 701-708
DOI: 10.1055/s-0033-1343478
Review
© Georg Thieme Verlag KG Stuttgart · New York

Anti-atherogenic Effects of 17β-Estradiol

I. Resanovic
1   Laboratory of Radiobiology and Molecular Genetics, Institute Vinca, University of Belgrade, Belgrade, Serbia
,
M. Rizzo
2   BioMedical Department of Internal Medicine and Medical Specialties, University of Palermo, Italy
3   Euro-Mediterranean Institute of Science and Technology, Italy
,
S. Zafirovic
1   Laboratory of Radiobiology and Molecular Genetics, Institute Vinca, University of Belgrade, Belgrade, Serbia
,
P. Bjelogrlic
4   School of Medicine, University of St. Andrews, St. Andrews, Scotland, UK
,
M. Perovic
5   University Clinic of Gynecology and Obstetrics “Narodni front”, University of Belgrade, Belgrade, Serbia
,
K. Savic
1   Laboratory of Radiobiology and Molecular Genetics, Institute Vinca, University of Belgrade, Belgrade, Serbia
,
A. M. Patti
6   BioMedical Department of Internal Medicine and Medical Specialties, ­University of Palermo, Italy
,
R. E. Isenovic
1   Laboratory of Radiobiology and Molecular Genetics, Institute Vinca, University of Belgrade, Belgrade, Serbia
› Author Affiliations
Further Information

Publication History

received 16 November 2012

accepted 02 April 2013

Publication Date:
16 May 2013 (online)

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Abstract

Estrogens are secreted primarily by the ovaries and placenta, by the testes in men and also produced by peripheral steroidogenic conversion. The 3 major naturally occurring estrogens are: 17β-estradiol (E2), estrone and estriol, of which E2 is the predominant and most active. The actions of E2 are mediated by at least 3 different receptors – the classical ERs (ERα and ERβ) and G-protein coupled receptor 30 (GPR30). E2 signaling in cardiomyocytes involves ERα- and ERβ-independent pathways, and treatment with the E2 receptor antagonists (Selective Estrogen Receptor Modulators- SERMs), which are agonists of GPR30, inhibits cardiac cell growth. Effects of E2 in preventing endothelial dysfunction, a prerequisite of atherosclerosis, are well recognized. Atherosclerosis involves interaction between the cells of the arterial wall endothelial cells (EC) and vascular smooth muscle cell (VSMC), as well as migration of macrophages into wall tunica media. It is predominantly developed at sites with abnormally high shear stress, such as bifurcations or branching of arteries, initiated by an injury to the endothelium and exposure to atherogenic lipids and toxins, such as those contained in tobacco smoke or infectious agents. Animal studies have shown effects of E2 in preventing atherosclerosis, inflammation and endothelial or vascular dysfunction. Gender differences along this pathogenic pathway have been also described. We review the data from the available animal and human studies, which focus on anti-atherogenic effects of E2. These studies represent evidence, albeit indirect, for an inhibitory effect of E2 on the progression of coronary artery atherosclerosis.