Many studies have proven that estrogens not only regulate functioning of the cardiovascular system, but also affect the risk of developing cardiovascular diseases.

Estrogens have local and systemic effects on the cardiovascular system. Signaling to a number of the cells of vascular walls and myocardium by estrogens is accomplished through genomic and non-genomic effects with the use of estrogen receptors. Estrogents bind to their three designanted estrogen receptors – ER?, ER?, and G protein-coupled estrogen receptor 1 (GPER1) (2).
Estrogen receptors are present in the heart and blood vessels, which confirms the that the cardiovascular system is the target organ for the action of estrogens. The effects of estrogens resulting on gene expression changes are called “genomic”. However, estrogen-dependent signaling pathways and functioning of estrogen receptors are much more complicated. It was determined that estrogen receptors of the vessels can be transcriptionally activated without being connected to estrogen directly, but rather through direct phosphorylation of the receptor by various kinases (ligand-independent activation of the receptor) (2).
Numerous studies have determined that estrogens participate in slowing the development of cardiac hypertrophy. Although, the mechanism by which this is being accomplished is still not completely understood, according to the most accepted theory estrogens prevent cardiac hypertrophy through estrogen mediated degradation of calcineurin A (2).
Cardiovascular health cannot be imagined without endothelial homeostasis, and endothelial dysfunction always leads to higher risks of cardiovascular pathologies. Rapid activation of eNOS (endothelial nitric oxide synthase) is an essential tool used for vascular relaxation, migration of endothelial cells, and proliferation. Another effect that estrogens receptors have on cardiovascular system is through nongenomic signaling pathway that allows to modulate intracellular calcium homeostasis at abnormally low estrogen concentration resulting in a rapid increase in intracellular calcium (1). Thus, estrogens signaling targets cardiovascular system and modulates proliferation of endothelic cells, migration, and vascular relaxation, preventing cardiac hypertrophy and attenuating histological damage after ischemia–reperfusion (I/R) injury. Imbalance of estrogens signaling results in cardiovascular diseases.

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