Evidence map›Paper›PMID 40492577›Full record

ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025

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

Zongwen Liang, Jinming Liu, Yanling Gou, Honglin Wang, Zhi Li, Yingying Cao, Huiyan Zhang, Ruru Bai, Zongfeng Zhang

Abstract read
In one paragraph

Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Zongwen LiangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.ORCID https://orcid.org/0000-0001-9387-6420
Jinming LiuDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yanling GouDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Honglin WangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Zhi LiDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Yingying CaoDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Huiyan ZhangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Ruru BaiDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.
Zongfeng ZhangDepartment of Obstetrics and Gynecology, The Second Affiliated Hospital of Harbin Medical University, Harbin, 150086, China.ORCID https://orcid.org/0000-0002-0159-1290

Funding

National Natural Science Foundation of China 82071619National Natural Science Foundation of China 82371654Natural Science Foundation of Heilongjiang Province PL2024H088
6 · The paper itself

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.

Indexed as

EndometriosisFerroptosisHeme Oxygenase-1HistonesHypoxia-Inducible Factor 1, alpha SubunitMethyltransferasesAnimalsDeoxyglucoseEndometriumFemaleHumansMiceSignal TransductionStromal CellsDeoxyglucoseHeme Oxygenase-1HIF1A protein, humanHistonesHypoxia-Inducible Factor 1, alpha SubunitMethyltransferasesendometriosisferroptosishif1ahistone lactylationhmox1mettl3

Identifiers

PMID40492577
PMCPMC12376633

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.