Evidence map›Paper›PMID 38639888›Full record

ArticleHormones (Athens, Greece)2024

The effect of GnRH-a on the angiogenesis of endometriosis.

Theodoros Filindris, Efthymia Papakonstantinou, Maria Keramida, Eleftherios Panteris, Sotiris Kalogeropoulos, Neoklis Georgopoulos, Fuminori Taniguchi, George Adonakis, Tasuku Harada, Apostolos Kaponis

Registry-linked trialOpen access · hybridAbstract read
In one paragraph

Article in Hormones (Athens, Greece), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06106932 (The Effects of GnRH-a on Angiogenesis of Endometriosis), which is not on this map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
5.4field-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.

NCT06106932 nacompletednot on this map

The Effects of GnRH-a on Angiogenesis of Endometriosis

TypeinterventionalSponsorUniversity of PatrasRan2015 to 2023Enrolled60ConditionsAngiogenesis, EndometriosisArmsLeuprolide Acetate
3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Trial
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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

10 authors at 3 institutions in 2 countries.

Theodoros FilindrisDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece.
Efthymia PapakonstantinouDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece.
Maria KeramidaDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece.
Eleftherios PanterisLaboratory of Forensic Medicine and Toxicology, School of Medicine, Aristotle University of Thessaloniki, Thessaloniki, 54124, Greece.
Sotiris KalogeropoulosDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece.
Neoklis GeorgopoulosDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece.
Fuminori TaniguchiDept. of Obstetrics & Gynecology, Tottori University Faculty of Medicine, Yonago, Japan.
George AdonakisDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece.
Tasuku HaradaDept. of Obstetrics & Gynecology, Tottori University Faculty of Medicine, Yonago, Japan.
Apostolos KaponisDept. of Obstetrics & Gynecology, Patras University School of Medicine, Patras, Greece. akaponis@upatras.gr.ORCID http://orcid.org/0000-0002-4738-2582
University of Patras · GRTottori University · JPAristotle University of Thessaloniki · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeNeoangiogenesis is necessary for adhesion and invasiveness of endometriotic lesions in women affected by endometriosis. Vascular endothelial growth factor (VEGF) is one of the main components of angiogenesis and is part of the major pathway tissue factor (TF)-protease activated receptor-2 (PAR-2)-VEGF that leads to neoangiogenesis. Specificity protein 1 (SP1) is a transcriptional factor that has recently been studied for its crucial role in angiogenesis via a specific pathway. We hypothesize that by blocking angiogenetic pathways we can suppress endometriotic lesions. Gonadotrophin-releasing hormone-agonists (GnRH-a) are routinely used, especially preoperatively, in endometriosis. It would be of great interest to clarify which angiogenetic pathways are affected and, thereby, pave the way for further research into antiangiogenetic effects on endometriosis.

methodsWe used quantitative real-time polymerase chain reaction (qRT-PCR) to study mRNA expression levels of TF, PAR-2, VEGF, and SP1 in endometriotic tissues of women who underwent surgery for endometriosis and received GnRH-a (leuprolide acetate) preoperatively.

resultsVEGF, TF, and PAR-2 expression is significantly lower in patients who received treatment (p < 0,001) compared to those who did not, whereas SP1 expression is not altered (p = 0.779).

conclusionsGnRH-a administration does affect some pathways of angiogenesis in endometriotic lesions, but not all of them. Therefore, supplementary treatments that affect the SP1 pathway of angiogenesis should be developed to enhance the antiangiogenetic effect of GnRH-a in patients with endometriosis.

trial registrationClinicaltrial.gov ID: NCT06106932.

Indexed as

EndometriosisNeovascularization, PathologicVascular Endothelial Growth Factor AAdultAngiogenesisFemaleGonadotropin-Releasing HormoneHumansLeuprolideReceptor, PAR-2Sp1 Transcription FactorThromboplastinGonadotropin-Releasing HormoneLeuprolideReceptor, PAR-2SP1 protein, humanSp1 Transcription FactorThromboplastinVascular Endothelial Growth Factor AVEGFA protein, humanAngiogenesisEndometriosisGnRH-aSP1VEGF

Identifiers

PMID38639888
PMCPMC11436414
OpenAlexW4394957846

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Registered trials

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.