Evidence map›Paper›PMID 36542122›Full record

ReviewNaunyn-Schmiedeberg's archives of pharmacology2023

Focus on the role of NLRP3 inflammasome in the pathology of endometriosis: a review on molecular mechanisms and possible medical applications.

Elnaz Irandoost, Shaparak Najibi, Saba Talebbeigi, Saina Nassiri

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
4.6field-weighted citation impact, top 5% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. Review
  9. Endometriosis: An Immunologist's Perspective.International journal of molecular sciences · 2025
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Elnaz IrandoostDepartment of Gynecology and Obstetrics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.ORCID http://orcid.org/0000-0002-6292-7720
Shaparak NajibiDepartment of Gynecology and Obstetrics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Saba TalebbeigiDepartment of Gynecology and Obstetrics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Saina NassiriDepartment of Gynecology and Obstetrics, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran. saina.nassiri@gmail.com.ORCID http://orcid.org/0000-0001-8430-755X
Tehran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis (EMS) is a gynecological disease that leads to pathological conditions, which are connected to the initiation of pro-inflammatory cytokine production. Inflammation plays a vital role in the pathogenesis of EMS. The activation and formation of cytoplasmic inflammasome complexes is considered an important step of inflammation and a key regulator of pyroptosis, a form of cell death. NLR family pyrin domain containing 3 (NLRP3) inflammasome complex modulates innate immune activity and inflammation. The NLRP3 inflammasome activates cysteine protease caspase-1, which produces active pro-inflammatory interleukins (ILs), including IL-1β and IL-18. The aim of this review article was to discuss the involvement of NLRP3 inflammasome assembly and its activation in the pathophysiology of EMS and target related pathways in designing appropriate therapeutic approaches. Dysregulation of sex hormone signaling pathways was associated with over-activation of the NLPR3 inflammasome. In this study, we demonstrated the involvement of NLRP3 inflammasome signaling pathways in the pathophysiology of EMS. The manuscript also discusses the beneficial effects of targeted therapy through synthetic inhibitors of NLRP3 signaling pathways to control EMS lesions.

Indexed as

EndometriosisInflammasomesFemaleHumansInflammationInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinEndometriosisInflammasomeInflammationNLRP3Pro-inflammatory cytokine

Identifiers

PMID36542122
OpenAlexW4312066333

What OpenQuestion holds

Textmetadata
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.