Evidence map›Paper›PMID 35853978›Full record

ArticleScientific reports2022

SIRT1 upregulation promotes epithelial-mesenchymal transition by inducing senescence escape in endometriosis.

Minghua Wang, Yongqi Wu, Yunbiao He, Jing Liu, Yingxing Chen, Jieqiong Huang, Guolong Qi, Ping Li

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.8field-weighted citation impact, top 2% of its field
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

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Research Progress of Histone Deacetylase and Its Inhibitors in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Sirtuins in Women's Health.Pharmaceuticals (Basel, Switzerland) · 2025
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Endometriosis and the Risk of Melanoma: A Shared Thread?Journal of obstetrics and gynaecology of India · 2024
    Article
  17. Article
  18. Article
  19. Review
  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

8 authors at 2 institutions in 1 country.

Minghua WangDepartment of Pathology, Longgang District People's Hospital, Shenzhen, 518172, China.
Yongqi WuDepartment of Pathology, Jinan University School of Medicine, Guangzhou, 510632, China.
Yunbiao HeDepartment of Medical Statistics, Jinan University School of Medicine, Guangzhou, 510632, China.
Jing LiuDepartment of Pathology, Jinan University School of Medicine, Guangzhou, 510632, China.
Yingxing ChenDepartment of Gynecology and Obstetrics, First Affiliated Hospital of Jinan University, Guangzhou, 510630, China.
Jieqiong HuangDepartment of Pathology, Jinan University School of Medicine, Guangzhou, 510632, China.
Guolong QiDepartment of Medical Statistics, Jinan University School of Medicine, Guangzhou, 510632, China. qijacky1976@hotmail.com.
Ping LiDepartment of Pathology, Jinan University School of Medicine, Guangzhou, 510632, China. pinger355@126.com.
Jinan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometrial epithelial cells carry distinct cancer-associated alterations that may be more susceptible to endometriosis. Mouse models have shown that overexpression of SIRT1 associated with oncogene activation contributes to the pathogenesis of endometriosis, but the underlying reason remains elusive. Here, we used integrated systems biology analysis and found that enrichment of endometrial stromal fibroblasts in endometriosis and their cellular abundance correlated negatively with epithelial cells in clinical specimens. Furthermore, endometrial epithelial cells were characterized by significant overexpression of SIRT1, which is involved in triggering the EMT switch by escaping damage or oncogene-induced induced senescence in clinical specimens and in vitro human cell line models. This observation supports that genetic and epigenetic incident favors endometrial epithelia cells escape from senescence and fuel EMT process in endometriosis, what could be overcome by downregulation of SIRT1.

Indexed as

EndometriosisSirtuin 1AnimalsEndometriumEpithelial-Mesenchymal TransitionFemaleHumansMiceUp-RegulationSIRT1 protein, humanSirt1 protein, mouseSirtuin 1

Identifiers

PMID35853978
PMCPMC9296487
OpenAlexW4285794766

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.