Figure 3 Mechanisms by which oestradiol reduces

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Figure 3 Mechanisms by which oestradiol reduces endothelial dysfunction and promotes cardiomyocyte protection Figure 3 | Mechanisms by which oestradiol reduces endothelial dysfunction and promotes cardiomyocyte protection. a | In cardiomyocytes, oestradiol (acting through oestrogen receptors (ERs)) inhibits angiotensin II (AGTII)-mediated effects, such as activation of phosphoinositide 3-kinase (PI3K) and calcineurin (CaN)-dependent transcription of genes encoding hypertrophic proteins, which has a direct antihypertrophic effect. Oestradiol also induces cardiomyocyte protection, through activation of the PI3K–protein kinase B (PKB) and p38 mitogen-activated protein kinase (MAPK) pathways, which prevents the generation of reactive oxygen species (ROS) and inhibits apoptosis. In addition, oestradiol activates sirtuin 1 (SIRT1), which inhibits AGTII-induced ROS production, cardiomyocyte hypertrophy and apoptosis. Oestradiol also downregulates the expression of microRNA-22 (miR-22) via ERα, which leads to the upregulation of the transcription factor Sp1 in cardiomyocytes. Sp1 increases the expression of cardioprotective genes, such as the gene that encodes cystathionine-γ-lyase (CTH), which increases the levels of hydrogen sulfide (H2S), which enhances the protection of cardiomyocytes from ROS. Cardiovascular protection also occurs following activation of G protein-coupled oestrogen receptor 1 (GPER1), which is mediated by the highly specific GPER1 agonist G1 through a PI3K-dependent mechanism. b | Exposure to a physiological concentration of oestradiol reduces the pro-inflammatory activation of vascular endothelial cells, reducing the production of IL-6 and IL-8 and the expression of vascular cell adhesion molecule 1 (VCAM1) and intercellular adhesion molecule 1 (ICAM1), which are involved in recruitment of leukocytes, thus preventing the development of atherosclerosis. In addition, oestradiol stimulates endothelial recovery in conditions of vascular injury by promoting, through genomic and non-genomic pathways, the activation of endothelial nitric oxide synthase (eNOS), which facilitates vasodilation. Although details of the pathway have been identified, the exact mechanisms by which eNOS is activated by oestradiol have not been completely elucidated. Oestradiol also alters the lipoprotein profile, which increases the amount of HDL. HDL stimulates the production of NO via scavenger receptor B, type I (SRBI)-mediated activation of eNOS to result in vasodilation. Solid lines indicate direct effects of the indicated proteins on the targets. Dashed lines define pathways that have not completely been elucidated yet. CaM, calmodulin; ERE, oestrogen-responsive element; HSP90, heat shock protein 90. Morselli, E. et al. (2017) The effects of oestrogens and their receptors on cardiometabolic health Nat. Rev. Endocrinol. doi:10.1038/nrendo.2017.12