Evidence map›Paper›PMID 33435569›Full record

ReviewBiomedicines2021

Inflammatory Mediators and Pain in Endometriosis: A Systematic Review.

Nikolaos Machairiotis, Sofia Vasilakaki, Nikolaos Thomakos

Open access · goldAbstract readReview
In one paragraph

Review in Biomedicines, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed, 3 pooled it
18.3field-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

90 citing papers in PubMed, 3 syntheses or guidelines pooled it, 144 citations in OpenAlex.

  1. Pooled it
  2. Prolactin and pain of endometriosis.Pharmacology & therapeutics · 2023
    Pooled it
  3. Pooled it
  4. Altered Blood Pressure Reflexes in Women With Endometriosis.Hypertension (Dallas, Tex. : 1979) · 2025
    Trial
  5. Review
  6. Review
  7. Identification of potent inhibitors of JUN N-terminal kinases for treatment of endometriosis and associated pain.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Review
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  11. Article
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  19. Article
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30 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

3 authors at 2 institutions in 2 countries.

Nikolaos MachairiotisDepartment of Obstetrics and Gynaecology, Accredited Endometriosis Centre, Northwick Park Hospital, London North West University Healthcare, London HA1 3UJ, UK.ORCID 0000-0003-2260-9709
Sofia VasilakakiDepartment of Pharmaceutical Chemistry, School of Pharmacy, University of Athens, Panepistimiopolis Zografou, 157 71 Athens, Greece.ORCID 0000-0002-1008-7264
Nikolaos Thomakos1st Department of Obstetrics and Gynecology, Alexandra Hospital, Gynecologic Oncology Unit, National and Kapodistrian University of Athens, 115 28 Athens, Greece.
National and Kapodistrian University of Athens · GRLondon North West Healthcare NHS Trust · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundpain is one of the main symptoms of endometriosis and it has a deleterious effect on a patients' personal and social life. To date, the clinical management of pain includes prolonged medication use and, in some cases, surgery, both of which are disruptive events for patients. Hence, there is an urgency for the development of a sufficient non-invasive medical treatment. Inflammation is one of the causative factors of pain in endometriosis. It is well established that inflammatory mediators promote angiogenesis and interact with the sensory neurons inducing the pain signal; the threshold of pain varies and it depends on the state and location of the disease. The inhibition of inflammatory mediators' synthesis might offer a novel and effective treatment of the pain that is caused by inflammation in endometriosis.

objectivespatients with endometriosis experience chronic pelvic pain, which is moderate to severe in terms of intensity. The objective of this systematic review is to highlight the inflammatory mediators that contribute to the induction of pain in endometriosis and present their biological mechanism of action. In addition, the authors aim to identify new targets for the development of novel treatments for chronic pelvic pain in patients with endometriosis. DATA SOURCES: three databases (PubMed, Scopus, and Europe PMC) were searched in order to retrieve articles with the keywords 'inflammation, pain, and endometriosis' between the review period of 1 January 2016 to 31 December 2020. This review has been registered with PROSPERO (registry number: CRD42020171018). Eligibility Criteria: only original articles that presented the regulation of inflammatory mediators and related biological molecules in endometriosis and their contribution in the stimulation of pain signal were included. DATA EXTRACTION: two authors independently extracted data from articles, using predefined criteria.

resultsthe database search yielded 1871 articles, which were narrowed down to 56 relevant articles of interest according to the eligibility criteria.

conclusionsinflammatory factors that promote angiogenesis and neuroangiogenesis are promising targets for the treatment of inflammatory pain in endometriosis. Specifically, CXC chemokine family, chemokine fractalkine, and PGE

Indexed as

cytokinesendometriosisinflammationneuroangiogenesispain

Identifiers

PMID33435569
PMCPMC7826862
OpenAlexW3118357284

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.