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. 2019 Sep 20;10:622. doi: 10.3389/fendo.2019.00622

Figure 2.

Figure 2

Interactions between estrogen signaling, androgen signaling, and osteogenic signaling in vascular smooth muscle or aortic valve interstitial cells exposed to physiological levels of sex hormones. Note that—in general—both estrogens and androgens suppress osteogenic signaling via both genomic and non-genomic mechanisms in both cell types at physiological levels in relatively early to mid-life stages. Importantly, the therapeutic harnessing of these mechanisms requires substantial research into the context dependence of sex hormone signaling (e.g., timing relative to menopause, level to which hormones should be restored for optimal therapeutic benefit, etc.). TGF-β, transforming growth factor β; BMP, bone morphogenetic protein; Wnt, wingless-related integration site; TGFβR1/2, transforming growth factor beta receptor 1 or 2; BMPR1/2, bone morphogenetic protein receptor 1 or 2; Nox4, NADPH oxidase 4; SARA, smad anchor for receptor activation; Smad, Suppressor of Mothers Against Decapentaplegic; LRP5/6, Low-density lipoprotein receptor-related protein 5 or 6; CK1, Casein kinase 1; DVL, Disheveled protein; Axin, Axin 1 protein; APC, adenomatous polyposis coli protein; GSK3, Glycogen synthase kinase 3; CTTNβ, beta-catenin protein; TCF 4/7, Transcription factor 4 or 7; LEF1, Lymphoid Enhancer Binding Factor 1; FZD, Frizzled receptor.