Estrogen receptors mediate numerous favorable effects on cells and molecules implicated in
vascular inflammation and atherogenic process. However, harmful effects have also been suggested.
Actually, premenopausal women have a significantly lower risk for cardiovascular disease compared
to postmenopausal women or age matched males while the incidence of cardiovascular disease is
greater in postmenopausal than premenopausal women of the same age. The balance between the expression
of ER subtypes may play an important role in the paradoxical characterization of estrogens as
both beneficial and harmful. The activation of the newly discovered estrogen receptor GPR30 appears
to be of great potential as therapeutic target in coronary heart disease, though the signaling mechanisms mediated GPR30
function still have not fully elucidated. The aim of this review is to summarize the current state of knowledge on the role
of each estrogen receptor subtype in mediating the direct estrogen actions on different cellular components that participate
in the atherosclerotic inflammatory process. We hope this knowledge will shed some light on the cause of the paradoxical
characterization of estrogens as both beneficial and harmful, and advance the research in the development of specific ERagonists/
antagonists with improved benefit/risk ratio.
Keywords: Atherosclerosis, endothelial cells, estrogen receptor alpha, estrogen receptor beta, GPR-30, vascular inflammation,
vascular smooth muscle cells.
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