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. 2019 Jul 3;10:442. doi: 10.3389/fendo.2019.00442

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Copyright © 2019 Sickinghe, Korporaal, den Ruijter and Kessler.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The influence of E2 on (perivascular) fibrosis formation. (Perivascular) fibrosis formation is attenuated in women through E2-induced inhibition of collagen production. However, E2 receptor dimerization promotes fibrosis formation in men. GPR30 localization in men results in perivascular fibrosis formation, while GPR30 localization at the plasma membrane inhibits fibrosis formation in women. Yellow circles indicated with a “P” represent phosphorylated serine residues. ER-α is phosphorylated at Ser-118, while ER-β is phosphorylated at Ser108. Ang II, angiotensin II; AR, androgen receptor; ARE, androgen responsive element; ATR, angiotensin II receptor; Co-R, co-receptor; E2, 17β-estradiol; ER, estrogen receptor; ERE, ααestrogen responsive element; GPR30, G protein coupled receptor 30; iNOS, inducible nitric oxide synthase; RAMP3, receptor activity modifying protein 3; TGF-β, transforming growth factor-β.