Evidence map›Paper›PMID 29038523›Full record

ArticleScientific reports2017

Angiotensin II type 2 receptor (AT2R) as a novel modulator of inflammation in rheumatoid arthritis synovium.

Riccardo Terenzi, Mirko Manetti, Irene Rosa, Eloisa Romano, Felice Galluccio, Serena Guiducci, Lidia Ibba-Manneschi, Marco Matucci-Cerinic

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
3.8field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

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  3. RNA Interference Ex Vivo.Methods in molecular biology (Clifton, N.J.) · 2024
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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

8 authors at 2 institutions in 1 country.

Riccardo TerenziDepartment of Experimental and Clinical Medicine, Section of Internal Medicine, Rheumatology Unit, Azienda Ospedaliero-Universitaria Careggi (AOUC), University of Florence, Florence, Italy.
Mirko ManettiDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy. mirko.manetti@unifi.it.ORCID 0000-0003-3956-8480
Irene RosaDepartment of Experimental and Clinical Medicine, Section of Internal Medicine, Rheumatology Unit, Azienda Ospedaliero-Universitaria Careggi (AOUC), University of Florence, Florence, Italy.
Eloisa RomanoDepartment of Experimental and Clinical Medicine, Section of Internal Medicine, Rheumatology Unit, Azienda Ospedaliero-Universitaria Careggi (AOUC), University of Florence, Florence, Italy.
Felice GalluccioDepartment of Experimental and Clinical Medicine, Section of Internal Medicine, Rheumatology Unit, Azienda Ospedaliero-Universitaria Careggi (AOUC), University of Florence, Florence, Italy.
Serena GuiducciDepartment of Experimental and Clinical Medicine, Section of Internal Medicine, Rheumatology Unit, Azienda Ospedaliero-Universitaria Careggi (AOUC), University of Florence, Florence, Italy.
Lidia Ibba-ManneschiDepartment of Experimental and Clinical Medicine, Section of Anatomy and Histology, University of Florence, Florence, Italy.
Marco Matucci-CerinicDepartment of Experimental and Clinical Medicine, Section of Internal Medicine, Rheumatology Unit, Azienda Ospedaliero-Universitaria Careggi (AOUC), University of Florence, Florence, Italy.
Azienda Ospedaliero-Universitaria Careggi · ITUniversity of Florence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite increasing evidence suggesting that angiotensin II type 2 receptor (AT2R) may regulate tissue inflammation, no study has yet analyzed its possible implication in rheumatoid arthritis (RA) synovitis. In this study, we investigated the expression and function of AT2R in synovial tissue and cultured fibroblast-like synoviocytes (FLS) from RA patients. AT2R expression was strongly increased in RA compared with osteoarthritis (OA) synovium, as well as in in cultured RA-FLS respect to OA-FLS and healthy FLS. Treatment with pro-inflammatory cytokines was able not only to boost AT2R expression in RA-FLS and OA-FLS, but also to induce its de novo expression in healthy FLS. The stimulation of AT2R with the specific agonist CGP42112A significantly reduced gene expression of interleukin (IL)-1β and IL-6 and activation of NF-κB in RA-FLS, while opposite effects were elicited by AT2R small interfering RNA. Moreover, AT2R agonism efficiently decreased RA-FLS proliferation and migration either at baseline or under pro-inflammatory cytokine challenge. In conclusion, AT2R is strongly expressed in key effector cells of rheumatoid synovitis, namely RA-FLS, and the activation of AT2R with a specific agonist may effectively dampen their pro-inflammatory and aggressive behavior. AT2R agonism might represent a novel therapeutic strategy for patients with RA.

Indexed as

Arthritis, RheumatoidBiomarkersCell MovementCell ProliferationCytokinesFemaleFibroblastsFluorescent Antibody TechniqueGene ExpressionHumansImmunohistochemistryInflammation MediatorsMaleNF-kappa BOsteoarthritisReceptor, Angiotensin, Type 2BiomarkersCytokinesInflammation MediatorsNF-kappa BReceptor, Angiotensin, Type 2

Identifiers

PMID29038523
PMCPMC5643391
OpenAlexW2762605625

What OpenQuestion holds

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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.