Evidence map›Paper›PMID 31507610›Full record

ArticleFrontiers in immunology2019

Interleukin-1/-33 Signaling Pathways as Therapeutic Targets for Endometriosis.

Toru Kato, Koubun Yasuda, Kazufumi Matsushita, Ken J Ishii, Seiichi Hirota, Tomohiro Yoshimoto, Hiroaki Shibahara

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
  2. Article
  3. The role of IL-33/ST2 signaling in female reproductive diseases.Frontiers in cell and developmental biology · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Review
  16. The long road of drug development for endometriosis - Pains, gains, and hopes.Journal of controlled release : official journal of the Controlled Release Society · 2024
    Review
  17. Article
  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

7 authors at 1 institution in 1 country.

Toru KatoDepartment of Obstetrics and Gynecology, Hyogo College of Medicine, Nishinomiya, Japan.
Koubun YasudaDepartment of Immunology, Hyogo College of Medicine, Nishinomiya, Japan.
Kazufumi MatsushitaDepartment of Immunology, Hyogo College of Medicine, Nishinomiya, Japan.
Ken J IshiiDivision of Vaccine Science, Department of Microbiology and Immunology, The Institute of Medical Science, University of Tokyo, Tokyo, Japan.
Seiichi HirotaDepartment of Surgical Pathology, Hyogo College of Medicine, Nishinomiya, Japan.
Tomohiro YoshimotoDepartment of Immunology, Hyogo College of Medicine, Nishinomiya, Japan.
Hiroaki ShibaharaDepartment of Obstetrics and Gynecology, Hyogo College of Medicine, Nishinomiya, Japan.
Hyogo Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is an estrogen-dependent disease with symptoms of dysmenorrhea, chronic pain, and infertility that affects 6-10% of women of reproductive age. Medical or surgical therapy, such as administration of an anti-gonadotropin or ovarian cystectomy, provide effective pain relief. However, neither therapy can be used for patients wishing to become pregnant. Despite the high morbidity, the pathogenesis of endometriosis has not been well-elucidated. Several inflammatory cytokines are reported to participate in the onset of endometriosis. Here, we examined the role of interleukin (IL)-1/IL-33 signaling in the development of endometriosis using a mouse model of endometriosis. Endometriotic lesion volume was significantly reduced in

Indexed as

Signal TransductionAnimalsCytokinesDisease Models, AnimalDisease ProgressionDisease SusceptibilityEndometriosisFemaleInterleukin-1Interleukin-33MiceMice, KnockoutMolecular Targeted TherapyMyeloid Differentiation Factor 88CytokinesInterleukin-1Interleukin-33Myeloid Differentiation Factor 88estrogenIL-1R1IRAK4MyD88ST2

Identifiers

PMID31507610
PMCPMC6714064
OpenAlexW2968681366

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.