Evidence map›Paper›PMID 30140375›Full record

ArticleOncotarget2018

Absence of formyl peptide receptor 1 causes endometriotic lesion regression in a mouse model of surgically-induced endometriosis.

Roberta Fusco, Ramona D'amico, Marika Cordaro, Enrico Gugliandolo, Rosalba Siracusa, Alessio Filippo Peritore, Rosalia Crupi, Daniela Impellizzeri, Salvatore Cuzzocrea, Rosanna Di Paola

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.2field-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

40 citing papers in PubMed, 53 citations in OpenAlex.

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  16. Key Mechanisms and Potential Implications ofAntioxidants (Basel, Switzerland) · 2021
    Article
  17. Article
  18. Article
  19. HidroxAntioxidants (Basel, Switzerland) · 2021
    Article
  20. Autophagy and Mitophagy Promotion in a Rat Model of Endometriosis.International journal of molecular sciences · 2021
    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

10 authors at 2 institutions in 2 countries.

Roberta FuscoDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Ramona D'amicoDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Marika CordaroDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Enrico GugliandoloDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Rosalba SiracusaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Alessio Filippo PeritoreDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Rosalia CrupiDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Daniela ImpellizzeriDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Salvatore CuzzocreaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
Rosanna Di PaolaDepartment of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Messina, Italy.
University of Messina · ITSaint Louis University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a female disease in which endometrial tissues grows outside the uterus. Patients showed alterations in endocrine and immune systems. Endometriotic lesions are characterized by deregulated interaction between immune cells and tissue cells. The formyl peptide receptor 1 (Fpr1) is expressed by both immune and stromal cells including epithelial cells. We investigated the development of the physiopathology of the surgically-induced endometriosis in Fpr1 KO mice compared to WT animals. Operated Fpr1 KO mice showed lower duration of uterine pain behaviors, lower size of developed cysts and reduced mast cell numbers. Immunohistochemical analyses indicated changes in NGF, VEGF and ICAM-1 expression associated with the pathology, which were reduced in absence of the Fpr1 gene. Molecular analyses indicated that in absence of Fpr1 there was reduced neutrophils accumulation and nitrosative stress formation, NF-κB translocation into the nucleus as well as NRLP3 inflammasome signalling. Fpr1 gene deletion caused reduction of resistance to the apoptosis, assessed by TUNEL assay. We underline the pathogenic role of Fpr1 in experimental endometriosis, which is the result of modulation of immune cell recruitment, suggesting it as a new target to control the pathologic features of endometriotic lesions.

Indexed as

endometriosisFpr1inflammasomeknockoutmouse

Identifiers

PMID30140375
PMCPMC6101131
OpenAlexW2886832879

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.