{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,11]],"date-time":"2026-06-11T05:52:03Z","timestamp":1781157123275,"version":"3.54.1"},"reference-count":44,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,6,24]],"date-time":"2025-06-24T00:00:00Z","timestamp":1750723200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:p>Endometriosis is a chronic inflammatory gynecological condition marked by the presence of tissue similar to the endometrium grows outside the uterus, often leading pelvic pain and infertility. This study explores how enhancer of zeste homolog 2 (EZH2) influences endometriosis, particularly through its interaction with estrogen receptors (ERs). We found that EZH2 reduces ER\u03b1 expression, allowing ER\u03b2 to bind to the tumor necrosis factor \u03b1 (TNF\u03b1) promoter and increase TNF\u03b1 levels, fueling inflammation. In mice, the EZH2 inhibitor GSK343 reduced TNF\u03b1 levels and endometriosis progression, similar to gene knockdown of ER\u03b2 or EZH2. In human samples, endometriotic tissue showed higher levels of\u00a0EZH2 and ER\u03b2 and lower levels of ER\u03b1 than in controls. Thus, EZH2 promotes\u00a0TNF\u03b1-driven inflammation, contributing to endometriosis. Targeting EZH2, as with GSK343, could be a promising therapeutic strategy for endometriosis treatment.<\/jats:p>","DOI":"10.3389\/fendo.2025.1574938","type":"journal-article","created":{"date-parts":[[2025,6,24]],"date-time":"2025-06-24T04:10:36Z","timestamp":1750738236000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":1,"title":["EZH2 promotes endometriosis progression through estrogen receptor and TNF\u03b1 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