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. 2019 Nov 10;20(22):5615. doi: 10.3390/ijms20225615

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Epigenetic mechanisms of hypermethylation and hypomethylation involved in the etiopathogenesis of endometriosis. Hypoxia and inflammation regulate DNA methylation through microRNAs (miRNA), and genes coding for three DNA methyltransferases (DNMT) were reported overexpressed in endometriosis. microRNAs (miRNA); DNA methyltransferases (DNMT); Homeobox A transcription factor (HOXA10); Progesterone receptor B (PR-B); 17β-hydroxysteroid dehydrogenase (17β-HSD); Steroidogenic factor-1 (SF-1); Estrogen receptor β (ER-β); Cyclo-oxygenase type 2 (COX-2); Prostaglandin E2 (P-E2); Estrogen (E); Progesterone (P).