Evidence map›Paper›PMID 26949527›Full record

ReviewF1000Research2016

Recent advances in the understanding of endometriosis: the role of inflammatory mediators in disease pathogenesis and treatment.

Warren Nothnick, Zahraa Alali

Open access · goldAbstract readReview
In one paragraph

Review in F1000Research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
10.6field-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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
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  9. Article
  10. Review
  11. Experimental and therapeutic medicine · 2021
    Article
  12. Article
  13. Review
  14. International journal of molecular sciences · 2020
    Review
  15. Purinergic Signaling in Endometriosis-Associated Pain.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Thalidomide Reduces Cell Proliferation in Endometriosis Experimentally Induced in Rats.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2019
    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

2 authors at 1 institution in 1 country.

Warren NothnickDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA; Institute for Reproductive Health and Regenerative Medicine, Center for Reproductive Sciences, University of Kansas Medical Center, Kansas City, KS, USA.
Zahraa AlaliDepartment of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA.
University of Kansas Medical Center · US

Funding

The Role of miR-451 in Endometriosis Pathophysiology and TreatmentR01HD069043 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NOTHNICK, WARREN B · 2012 to 2016
$1.7M
Dissecting the functional role of miRNAs in decidualizationR21HD073733 · NICHD · UNIVERSITY OF KANSAS MEDICAL CENTER · PI NOTHNICK, WARREN B · 2013 to 2014
$410k
NICHD NIH HHS R01 HD069043NICHD NIH HHS R21 HD073733
6 · The paper itself

Abstract

In this review, we focus on recent advancements in our understanding of the roles of inflammatory mediators in endometriosis pathophysiology and the potential for improved therapies based upon targeting these pathways. We review the association between endometriosis and inflammation and the initial promise of anti-tumor necrosis factor therapies based upon experimental evidence, and how and why these studies have not translated to the clinic. We then discuss emerging data on the role of inter-relationship among macrophage migration inhibitory factor, prostaglandin E 2, and estrogen receptor-beta, and the potential utility of targeting these factors in endometriosis treatment. In doing so, we highlight the strengths and discuss the current research on identification of novel, anti-inflammatory-based therapy and the necessity to expand experimental endpoints to include clinically relevant measures when assessing the efficacy of potential new therapies for endometriosis.

Indexed as

endometriosisestrogen receptor-betaprostaglandin E2

Identifiers

PMID26949527
PMCPMC4760268
OpenAlexW2286138571

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.