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Figure 1

Figure 1. Possible mechanisms responsible for estrogen-mediated vasodilatation, renal and cardiovascular protection. From: Estrogen, hormonal replacement therapy and cardiovascular disease.

The multifaceted mechanisms of estrogen involve (a) acting on estrogen receptor-α (ERα) and ERβ to reduce synthesis of NADPH oxidase and increase synthesis of endothelial nitric oxide synthase (eNOS) and superoxide dismutase (SOD), thereby decreasing superoxide and increasing NO production and bioavailability (genomic effect); (b) rapidly activating eNOS via a calcium-mediated mechanism(s) without altering gene expression (nongenomic effect), leading to NO/cGMP release and vascular relaxation; (c) activating Akt via MAP kinase (MAPK)–PI3 kinase (PI3K) pathways, reducing apoptosis and enhancing cell survival and (d) reducing NF-κB activation/translocation via p38α-mediated p53 phosphorylation and JNK1/2-mediated signaling pathways, inhibiting chemokine/cytokine transcription and decreasing inflammation. In addition, estrogen acts on the membrane-bound and G-protein-coupled estrogen receptor (GPER) GPR30 associated with transactivation of epidermal growth factor receptors, which induces rapid signal transduction, including activation of MAPK, protein kinase A (PKA) and PI3K, leading to cardiovascular protection.

Xiao-Ping Yang, et al. Curr Opin Nephrol Hypertens. ;20(2):133-138.

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