Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway

Abstract Endometriosis (EMs) is a chronic gynecologic condition characterized by the growth of endometrial stromal and glandular tissue outside the uterine cavity of unknown etiology. Currently, ferroptosis resistance, increased glycolysis, and increased lactate production are identified in EMs. His...

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Main Authors: Zongwen Liang, Jinming Liu, Yanling Gou, Honglin Wang, Zhi Li, Yingying Cao, Huiyan Zhang, Ruru Bai, Zongfeng Zhang
Format: Article
Language:English
Published: Wiley 2025-08-01
Series:Advanced Science
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Online Access:https://doi.org/10.1002/advs.202408220
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author Zongwen Liang
Jinming Liu
Yanling Gou
Honglin Wang
Zhi Li
Yingying Cao
Huiyan Zhang
Ruru Bai
Zongfeng Zhang
author_facet Zongwen Liang
Jinming Liu
Yanling Gou
Honglin Wang
Zhi Li
Yingying Cao
Huiyan Zhang
Ruru Bai
Zongfeng Zhang
author_sort Zongwen Liang
collection DOAJ
description Abstract Endometriosis (EMs) is a chronic gynecologic condition characterized by the growth of endometrial stromal and glandular tissue outside the uterine cavity of unknown etiology. Currently, ferroptosis resistance, increased glycolysis, and increased lactate production are identified in EMs. Histone lactylation is a lactate‐derived posttranslational modification that is recognized primarily for its role in epigenetic regulation. In this study, it is demonstrated that increased histone lactylation contributes to ferroptosis resistance in ectopic endometrial stromal cells (EESCs). Mechanistically, histone lactylation mediates ferroptosis resistance through the hypoxia‐inducible factor 1 alpha (HIF1A)/heme oxygenase 1 (HMOX1) signaling pathway, which is regulated by methyltransferase like 3 (METTL3). In vivo experiments reveal that combination therapy with 2‐deoxy‐D‐glucose (2‐DG) and erastin is more effective for the treatment of EMs. Together, the findings provide a theoretical basis for the pathogenesis of EMs and suggest that a combined treatment that inhibits histone lactylation and induces ferroptosis is an effective treatment for EMs.
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institution Kabale University
issn 2198-3844
language English
publishDate 2025-08-01
publisher Wiley
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series Advanced Science
spelling doaj-art-40c7a0197f1a4fddaac3146108169aa22025-08-23T14:15:01ZengWileyAdvanced Science2198-38442025-08-011231n/an/a10.1002/advs.202408220Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling PathwayZongwen Liang0Jinming Liu1Yanling Gou2Honglin Wang3Zhi Li4Yingying Cao5Huiyan Zhang6Ruru Bai7Zongfeng Zhang8Department of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaDepartment of Obstetrics and GynecologyThe Second Affiliated Hospital of Harbin Medical UniversityHarbin150086ChinaAbstract Endometriosis (EMs) is a chronic gynecologic condition characterized by the growth of endometrial stromal and glandular tissue outside the uterine cavity of unknown etiology. Currently, ferroptosis resistance, increased glycolysis, and increased lactate production are identified in EMs. Histone lactylation is a lactate‐derived posttranslational modification that is recognized primarily for its role in epigenetic regulation. In this study, it is demonstrated that increased histone lactylation contributes to ferroptosis resistance in ectopic endometrial stromal cells (EESCs). Mechanistically, histone lactylation mediates ferroptosis resistance through the hypoxia‐inducible factor 1 alpha (HIF1A)/heme oxygenase 1 (HMOX1) signaling pathway, which is regulated by methyltransferase like 3 (METTL3). In vivo experiments reveal that combination therapy with 2‐deoxy‐D‐glucose (2‐DG) and erastin is more effective for the treatment of EMs. Together, the findings provide a theoretical basis for the pathogenesis of EMs and suggest that a combined treatment that inhibits histone lactylation and induces ferroptosis is an effective treatment for EMs.https://doi.org/10.1002/advs.202408220endometriosisferroptosishif1ahistone lactylationhmox1mettl3
spellingShingle Zongwen Liang
Jinming Liu
Yanling Gou
Honglin Wang
Zhi Li
Yingying Cao
Huiyan Zhang
Ruru Bai
Zongfeng Zhang
Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway
Advanced Science
endometriosis
ferroptosis
hif1a
histone lactylation
hmox1
mettl3
title Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway
title_full Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway
title_fullStr Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway
title_full_unstemmed Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway
title_short Elevated Histone Lactylation Mediates Ferroptosis Resistance in Endometriosis Through the METTL3‐Regulated HIF1A/HMOX1 Signaling Pathway
title_sort elevated histone lactylation mediates ferroptosis resistance in endometriosis through the mettl3 regulated hif1a hmox1 signaling pathway
topic endometriosis
ferroptosis
hif1a
histone lactylation
hmox1
mettl3
url https://doi.org/10.1002/advs.202408220
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