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. 2020 May 16;26(4):565–585. doi: 10.1093/humupd/dmaa009

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© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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Hypothetical targets and strategies to overcome progesterone resistance in endometriosis based on currently available drugs. Progesterone receptor (PR) expression is inhibited by gene hypermethylation induced by proinflammatory cytokines and reactive oxygen species (ROS), which could be inhibited by anti-inflammatory drugs/immunomodulators and antioxidants, respectively. The same drugs and others, such as retinoids, may activate mechanisms downstream PR signalling that prevent endometriosis proliferation and fibrosis. Blue arrows: stimulation; red arrows: inhibition. ER: estrogen receptor; p-Akt: phosphorylated serine/threonine protein kinase B; p-ERK1/2: phosphorylated extracellular signal-regulated kinase 1/2; NF-κB: nuclear factor-kappa B; ADAM17: A disintegrin and metalloproteases metallopeptidase domain 17; TNF: tumour necrosis factor; IL: interleukin.