Evidence map›Paper›PMID 28508153›Full record

ReviewSeminars in immunopathology2017

Cellular and molecular perspectives in rheumatoid arthritis.

Douglas J Veale, Carl Orr, Ursula Fearon

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.1field-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

59 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
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  3. The Therapeutic Effects ofAntioxidants (Basel, Switzerland) · 2025
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  11. Combination treatment with interferon-γ may be a potential strategy to improve the efficacy of cytotherapy for rheumatoid arthritis: A network meta-analysis.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 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

3 authors at 2 institutions in 1 country.

Douglas J VealeThe Centre for Arthritis and Rheumatic Diseases, University College Dublin, Dublin 4, Ireland. douglas.veale@ucd.ie.ORCID 0000-0003-2802-4971
Carl OrrThe Centre for Arthritis and Rheumatic Diseases, University College Dublin, Dublin 4, Ireland.
Ursula FearonThe Department of Molecular Rheumatology, Trinity College Dublin, Dublin 2, Ireland.
University College Dublin · IETrinity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Synovial immunopathology in rheumatoid arthritis is complex involving both resident and infiltrating cells. The synovial tissue undergoes significant neovascularization, facilitating an influx of lymphocytes and monocytes that transform a typically acellular loose areolar membrane into an invasive tumour-like pannus. The microvasculature proliferates to form straight regularly-branching vessels; however, they are highly dysfunctional resulting in reduced oxygen supply and a hypoxic microenvironment. Autoantibodies such as rheumatoid factor and anti-citrullinated protein antibodies are found at an early stage, often before arthritis has developed, and they have been implicated in the pathogenesis of RA. Abnormal cellular metabolism and mitochondrial dysfunction thus ensue and, in turn, through the increased production of reactive oxygen species actively induce inflammation. Key pro-inflammatory cytokines, chemokines and growth factors and their signalling pathways, including nuclear factor κB, Janus kinase-signal transducer, are highly activated when immune cells are exposed to hypoxia in the inflamed rheumatoid joint show adaptive survival reactions by activating. This review attempts to highlight those aberrations in the innate and adaptive immune systems including the role of genetic and environmental factors, autoantibodies, cellular alterations, signalling pathways and metabolism that are implicated in the pathogenesis of RA and may therefore provide an opportunity for therapeutic intervention.

Indexed as

AnimalsArthritis, RheumatoidAutoantibodiesDisease SusceptibilityEnvironmentGenetic Predisposition to DiseaseHumansHypoxiaSignal TransductionSynovial MembraneAutoantibodiesAngiogenesisB-cellsFibroblastsHypoxiaRheumatoid arthritisSynovial tissueT-cells

Identifiers

PMID28508153
OpenAlexW2615710315

What OpenQuestion holds

Textmetadata
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.