Evidence map›Paper›PMID 32570986›Full record

ReviewJournal of clinical medicine2020

Epithelial-Mesenchymal Transition in Endometriosis-When Does It Happen?

Lutz Konrad, Raimund Dietze, Muhammad A Riaz, Georgios Scheiner-Bobis, Judith Behnke, Fabian Horné, Alena Hoerscher, Christoph Reising, Ivo Meinhold-Heerlein

Abstract readReview
In one paragraph

Review in Journal of clinical medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed, 1 pooled it
–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

64 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Article
  8. Exploring New Treatment Strategies for Endometriosis-Narrative Review.International journal of molecular sciences · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. IL-6 Inhibits Invasion in a Murine Model of Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2025
    Article
  18. Article
  19. Article
  20. Review

4 more citing papers are in PubMed but not listed here.

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.

Lutz KonradInstitute of Gynecology and Obstetrics, Faculty of Medicine, Justus Liebig University Giessen, 35392 Giessen, Germany.ORCID 0000-0001-5878-3050
Raimund DietzeInstitute of Molecular Biology and Tumor Research (IMT), Philipps University of Marburg, 35037 Marburg, Germany.
Muhammad A RiazInstitute of Gynecology and Obstetrics, Faculty of Medicine, Justus Liebig University Giessen, 35392 Giessen, Germany.
Georgios Scheiner-BobisInstitute for Veterinary-Physiology and -Biochemistry, School of Veterinary Medicine, Justus-Liebig-University, 35390 Gießen, Germany.
Judith BehnkeDepartment of General Pediatrics and Neonatalogy, Justus Liebig University Giessen, Universities of Giessen and Marburg Lung Center (UGMLC), Member of the German Center for Lung Research (DZL), 35392 Giessen, Germany.ORCID 0000-0003-4307-8759
Fabian HornéInstitute of Gynecology and Obstetrics, Faculty of Medicine, Justus Liebig University Giessen, 35392 Giessen, Germany.
Alena HoerscherInstitute of Gynecology and Obstetrics, Faculty of Medicine, Justus Liebig University Giessen, 35392 Giessen, Germany.
Christoph ReisingInstitute of Gynecology and Obstetrics, Faculty of Medicine, Justus Liebig University Giessen, 35392 Giessen, Germany.
Ivo Meinhold-HeerleinInstitute of Gynecology and Obstetrics, Faculty of Medicine, Justus Liebig University Giessen, 35392 Giessen, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial-mesenchymal transition (EMT) is an important process of cell remodeling characterized by the gradual loss of the epithelial phenotype and progressive gain of a mesenchymal phenotype. EMT is not an all-or-nothing process, but instead a transition of epithelial to mesenchymal cells with intermediate cell states. Recently, EMT was described in endometriosis, and many EMT-specific pathways like Twist, Snail, Slug, Zinc finger E-box-binding homeobox 1/2 (ZEB1/2), E/N-cadherin, keratins, and claudins are involved. However, as pointed out in this review, a comparison of the eutopic endometrium of women with and without endometriosis yielded only subtle changes of these EMT markers. Furthermore, only very few alterations in cell-cell contacts could be found but without changes in the epithelial phenotype. This suggests only a partial EMT which is not a prerequisite for the detachment of endometrial cells and, thus, not critical for the first step(s) in the pathogenesis of endometriosis. In contrast, the majority of changes in the EMT-related marker expression were found in the ectopic endometrium, especially in the three endometriotic entities, ovarian, peritoneal, and deep infiltrating endometriosis (DIE), compared with the eutopic endometrium. In this review, we examine the most important EMT pathways described in endometriosis and propose that partial EMT might result from the interaction of endometrial implants with their surrounding microenvironment.

Indexed as

cell–cell contactsendometriosisendometriumepithelial–mesenchymal transitionpathogenesis

Identifiers

PMID32570986
PMCPMC7357060

What OpenQuestion holds

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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.