Evidence map›Paper›PMID 31717614›Full record

ReviewInternational journal of molecular sciences2019

The Pathogenesis of Endometriosis: Molecular and Cell Biology Insights.

Antonio Simone Laganà, Simone Garzon, Martin Götte, Paola Viganò, Massimo Franchi, Fabio Ghezzi, Dan C Martin

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 246 papers, 10 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
246citing papers in PubMed, 10 pooled it
57.4field-weighted citation impact, top 1% 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

246 citing papers in PubMed, 10 syntheses or guidelines pooled it, 468 citations in OpenAlex.

  1. Pooled it
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  6. Endometriosis and COVID-19: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2022
    Pooled it
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  11. Trial
  12. Trial
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Exploring endometriosis through 3DMaterials today. Bio · 2026
    Review
  19. Review
  20. Review

186 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

7 authors at 5 institutions in 3 countries.

Antonio Simone LaganàDepartment of Obstetrics and Gynecology, "Filippo Del Ponte" Hospital, University of Insubria, Piazza Biroldi 1, 21100 Varese, Italy.ORCID 0000-0003-1543-2802
Simone GarzonDepartment of Obstetrics and Gynecology, "Filippo Del Ponte" Hospital, University of Insubria, Piazza Biroldi 1, 21100 Varese, Italy.ORCID 0000-0002-5840-699X
Martin GötteDepartment of Gynecology and Obstetrics, Münster University Hospital, D-48149 Münster, Germany.ORCID 0000-0003-2360-2496
Paola ViganòReproductive Sciences Laboratory, Division of Genetics and Cell Biology, San Raffaele Scientific Institute, Via Olgettina 60, 20136 Milan, Italy.
Massimo FranchiDepartment of Obstetrics and Gynecology, AOUI Verona, University of Verona, Piazzale Aristide Stefani 1, 37126 Verona, Italy.
Fabio GhezziDepartment of Obstetrics and Gynecology, "Filippo Del Ponte" Hospital, University of Insubria, Piazza Biroldi 1, 21100 Varese, Italy.
Dan C MartinSchool of Medicine, University of Tennessee Health Science Center, 910 Madison Ave, Memphis, TN 38163, USA.
University of Insubria · ITSan Raffaele University of Rome · ITUniversity Hospital Münster · DEUniversity of Tennessee Health Science Center · USUniversity of Verona · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The etiopathogenesis of endometriosis is a multifactorial process resulting in a heterogeneous disease. Considering that endometriosis etiology and pathogenesis are still far from being fully elucidated, the current review aims to offer a comprehensive summary of the available evidence. We performed a narrative review synthesizing the findings of the English literature retrieved from computerized databases from inception to June 2019, using the Medical Subject Headings (MeSH) unique ID term "Endometriosis" (ID:D004715) with "Etiology" (ID:Q000209), "Immunology" (ID:Q000276), "Genetics" (ID:D005823) and "Epigenesis, Genetic" (ID:D044127). Endometriosis may origin from Müllerian or non-Müllerian stem cells including those from the endometrial basal layer, Müllerian remnants, bone marrow, or the peritoneum. The innate ability of endometrial stem cells to regenerate cyclically seems to play a key role, as well as the dysregulated hormonal pathways. The presence of such cells in the peritoneal cavity and what leads to the development of endometriosis is a complex process with a large number of interconnected factors, potentially both inherited and acquired. Genetic predisposition is complex and related to the combined action of several genes with limited influence. The epigenetic mechanisms control many of the processes involved in the immunologic, immunohistochemical, histological, and biological aberrations that characterize the eutopic and ectopic endometrium in affected patients. However, what triggers such alterations is not clear and may be both genetically and epigenetically inherited, or it may be acquired by the particular combination of several elements such as the persistent peritoneal menstrual reflux as well as exogenous factors. The heterogeneity of endometriosis and the different contexts in which it develops suggest that a single etiopathogenetic model is not sufficient to explain its complex pathobiology.

Indexed as

Epigenesis, GeneticEndometriosisEndometriumFemaleHumansStem Cellsendometriosisepigeneticsgeneticsimmunologypathogenesis

Identifiers

PMID31717614
PMCPMC6888544
OpenAlexW2986294785

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.