Estrogen and the Vascular Injury Response

TLDR: In this chapter, vasoprotective actions of estrogen exerted at the level of the arterial wall will be considered in the context of balloon injury models and hypercholesterolemia.

Abstract: Gender plays an important role in the modulation of cardiovascular risk and events. Cardiovascular disease is less prevalent in premenopausal women than it is in age-matched men, but there is an increase in coronary risk and events in women after menopause (1). Although a prominent antiatherogenic response to estrogen is a reduction in plasma low density lipoprotein cholesterol (LDL-c) and an elevation of high density lipoprotein cholesterol (HDLc), other benefits are achieved by processes that are independent of changes in plasma lipid profiles (2–4). In this respect, estrogen therapy has proven to be effective in blunting the vascular injury response via both genomic and nongenomic mechanisms (5). Balloon injury of the rat carotid artery is an experimental paradigm that is commonly used to study mechanisms of atherogenesis. Estrogen minimizes the vascular injury response in this model through both direct antiproliferative effects and indirectly via the promotion of endothelial cell integrity and nitric oxide (NO) function (6–14). Additional protective effects of estrogen may be due to native antioxidant properties of the hormone (15). In this chapter, vasoprotective actions of estrogen exerted at the level of the arterial wall will be considered in the context of balloon injury models and hypercholesterolemia.