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. Author manuscript; available in PMC: 2011 Dec 1.
Published in final edited form as: J Cardiovasc Pharmacol. 2010 Dec;56(6):696–708. doi: 10.1097/FJC.0b013e3181f9ea8d

Figure 2. The potential role of estradiol metabolism in PAH.

Figure 2

(A) Activities of 2-hydroxylation, 16α-hydroxylation and 17β–HSD pathways determine the overall biological effects of E2 in PAH. (B) In endothelial cells, 2-methoxyestradiol (2ME) is a more potent modulator of prostacyclin, endothelin and nitric oxide synthesis/release than estradiol (E2); 2ME and E2 have opposite effects on endothelial pathobiology in PAH (2HE, 2-Hydroxyestradiol; 2ME1, 2-Methoxyestrone; E3, Estriol; 16αE1 , 16α–Estrone).