Evidence map›Paper›PMID 22146575›Full record

ArticleArthritis research & therapy2011

A2A and A3 adenosine receptor expression in rheumatoid arthritis: upregulation, inverse correlation with disease activity score and suppression of inflammatory cytokine and metalloproteinase release.

Katia Varani, Melissa Padovan, Fabrizio Vincenzi, Martina Targa, Francesco Trotta, Marcello Govoni, Pier Andrea Borea

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed
5.8field-weighted citation impact, top 4% 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

71 citing papers in PubMed, 135 citations in OpenAlex.

  1. Review
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  6. Gels (Basel, Switzerland) · 2025
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  15. Therapeutic Potential of Highly Selective AMolecules (Basel, Switzerland) · 2022
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  16. Article
  17. Adenosine and Inflammation: Here, There and Everywhere.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. AFrontiers in neuroscience · 2021
    Review

11 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

7 authors at 1 institution in 1 country.

Katia VaraniDepartment of Clinical and Experimental Medicine, Pharmacology Unit, University of Ferrara via Fossato di Mortara 17-19, 44121 Ferrara, Italy.
Melissa Padovan
Fabrizio Vincenzi
Martina Targa
Francesco Trotta
Marcello Govoni
Pier Andrea Borea
University of Ferrara · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionThe reduction of the inflammatory status represents one of the most important targets in rheumatoid arthritis (RA). A central role of A2A and A3 adenosine receptors (ARs) in mechanisms of inflammation has been reported in different pathologies. The primary aim of this study was to investigate the A2A and A3ARs and their involvement in RA progression measured by Disease Activity Score in 28 or 44 joints (DAS28 or DAS).

methodsARs were analyzed by saturation binding assays, mRNA and Western blotting analysis in lymphocytes from early and established RA patients. The effect of A2A and A3AR agonists in nuclear factor kB (NF-kB) pathway was evaluated. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) release was carried out by A2A and A3AR activation. AR pharmacological regulation in matrix metalloproteinase-1 (MMP-1) and metalloproteinase-3 (MMP-3) release was also studied.

resultsIn lymphocytes obtained from RA patients, A2A and A3ARs were up-regulated if compared with healthy controls. A2A and A3AR activation inhibited the NF-kB pathway and diminished inflammatory cytokines such as TNF-α, IL-1β and IL-6. A2A and A3AR agonists mediated a reduction of MMP-1 and MMP-3 release. A2A and A3AR density inversely correlated with DAS28 and DAS suggesting a direct role of the endogenous activation of these receptors in the control of RA joint inflammation.

conclusionsTaken together these data demonstrate that the inflammatory and clinical responses in RA are regulated by A2A and A3ARs and support the use of A2A and/or A3AR agonists as novel and effective pharmacological treatment in RA patients.

Indexed as

Gene ExpressionAdenosineAdenosine A2 Receptor AgonistsAgedArthritis, RheumatoidBlotting, WesternCells, CulturedCytokinesFemaleHumansInflammation MediatorsLinear ModelsLymphocytesMaleMetalloproteasesMiddle Aged2-(4-(2-carboxyethyl)phenethylamino)-5'-N-ethylcarboxamidoadenosine2-chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamideAdenosineAdenosine A2 Receptor AgonistsCytokinesInflammation MediatorsMetalloproteasesNF-kappa BPhenethylaminesReceptor, Adenosine A2AReceptor, Adenosine A3

Identifiers

PMID22146575
PMCPMC3334647
OpenAlexW2110418038

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.