Evidence map›Paper›PMID 29937493›Full record

ReviewInternational journal of molecular sciences2018

Pathogenomics of Endometriosis Development.

Vladislav Baranov, Olga Malysheva, Maria Yarmolinskaya

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
8.2field-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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. A new look at the theoretical causes of endometriosis: Narrative review.International journal of reproductive biomedicine · 2024
    Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Expression of Talin-1 in endometriosis and its possible role in pathogenesis.Reproductive biology and endocrinology : RB&E · 2021
    Article
  18. Article
  19. Article
  20. Article
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

3 authors at 1 institution in 1 country.

Vladislav BaranovD.O.Ott Institute of Obstetrics, Gynecology and Reproductology, Saint-Petersburg 199034, Russia. baranov@vb2475.spb.edu.
Olga MalyshevaD.O.Ott Institute of Obstetrics, Gynecology and Reproductology, Saint-Petersburg 199034, Russia. omal99@mail.ru.
Maria YarmolinskayaD.O.Ott Institute of Obstetrics, Gynecology and Reproductology, Saint-Petersburg 199034, Russia. m.yarmolinskaya@gmail.com.
Research Institute of Obstetrics and Gynecology named after D.O. Ott · RU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

For over 100 years, endometriosis, as a chronic, estrogen-dependent, inflammatory, heritable disease affecting approximately 5⁻10% of women in reproductive age has been the focus of clinicians and scientists. In spite of numerous environmental, genetic, epigenetic, endocrine, and immunological studies, our knowledge of endometriosis is still fragmentary, and its precise pathophysiology and pathogenomics remain a mystery. The implementation of new technologies has provided tremendous progress in understanding the many intrinsic molecular mechanisms in the development of endometriosis, with progenitor and stem cells (SCs) of the eutopic endometrium as the starting players and endometriotic lesions as the final pathomorphological trait. Novel data on the molecular, genetic, and epigenetic mechanisms of the disease are briefly outlined. We hypothesize the existence of an endometriosis development genetic program (EMDP) that governs the origin of endometrium stem cells programmed for endometriosis (1), their transition (metaplasia) into mesenchymal SCs (2), and their invasion of the peritoneum and progression to endometriotic lesions (3). The pros and cons of the recent unifying theory of endometriosis are also discussed. Complex genomic and epigenetic interactions at different stages of the endometriosis process result in different forms of the disease, with specific features and clinical manifestations. The significance of the EMDP in elaborating a new strategy for endometriosis prediction, prevention, and treatment is discussed.

Indexed as

Epigenesis, GeneticAdultCell DifferentiationCell MovementCytokinesEndometriosisEndometriumEpithelial-Mesenchymal TransitionFemaleHumansMesenchymal Stem CellsMicroRNAsNuclear ProteinsPeritoneumPluripotent Stem CellsProto-Oncogene Proteins c-bcl-2BCL2 protein, humanCytokinesMicroRNAsNuclear ProteinsProto-Oncogene Proteins c-bcl-2TWIST1 protein, humanTwist-Related Protein 1developmental pathwayendometriosismesenchymal stem cellspathogenomics

Identifiers

PMID29937493
PMCPMC6073754
OpenAlexW2809004298

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.