Evidence map›Paper›PMID 29579371›Full record

ReviewArthritis & rheumatology (Hoboken, N.J.)2018

Review: Synovial Cell Metabolism and Chronic Inflammation in Rheumatoid Arthritis.

Jane Falconer, Anne N Murphy, Stephen P Young, Andrew R Clark, Stefano Tiziani, Monica Guma, Christopher D Buckley

Open access · greenAbstract readReview
In one paragraph

Review in Arthritis & rheumatology (Hoboken, N.J.), 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 1 pooled it
23.5field-weighted citation impact, top 1% 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

188 citing papers in PubMed, 1 synthesis or guideline pooled it, 303 citations in OpenAlex.

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  13. The Application Prospects and Future Outlook ofDrug design, development and therapy · 2026
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128 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 5 institutions in 2 countries.

Jane FalconerUniversity of Birmingham, Queen Elizabeth Hospital and National Institute for Health Research, Birmingham Biomedical Research Centre, Birmingham, UK.
Anne N MurphyUniversity of California, San Diego.
Stephen P YoungUniversity of Birmingham, Queen Elizabeth Hospital and National Institute for Health Research, Birmingham Biomedical Research Centre, Birmingham, UK.
Andrew R ClarkUniversity of Birmingham, Queen Elizabeth Hospital, Birmingham, UK.
Stefano TizianiUniversity of Texas at Austin.
Monica GumaUniversity of California, San Diego.
Christopher D BuckleyUniversity of Birmingham, Queen Elizabeth Hospital, National Institute for Health Research, Birmingham Biomedical Research Centre, Birmingham, UK.
University of Birmingham · GBQueen Elizabeth Hospital · GBQueen Elizabeth Hospital Birmingham · GBThe University of Texas at Austin · USUniversity of Oxford · GB

Funding

Choline kinase: a novel target for rheumatoid arthritisK08AR064834 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUMA, MONICA · 2013 to 2017
$687k
Choline metabolites as biomarkers in rheumatoid arthritisR03AR068094 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI GUMA, MONICA · 2015 to 2018
$233k
Arthritis Research UK 19791Arthritis Research UK 20015Arthritis Research UK 20298Department of HealthNIAMS NIH HHS K08 AR064834NIAMS NIH HHS R03 AR068094Versus Arthritis 19791Versus Arthritis 20015Versus Arthritis 21226Versus Arthritis 21802Wellcome Trust
6 · The paper itself

Abstract

Metabolomic studies of body fluids show that immune-mediated inflammatory diseases such as rheumatoid arthritis (RA) are associated with metabolic disruption. This is likely to reflect the increased bioenergetic and biosynthetic demands of sustained inflammation and changes in nutrient and oxygen availability in damaged tissue. The synovial membrane lining layer is the principal site of inflammation in RA. Here, the resident cells are fibroblast-like synoviocytes (FLS) and synovial tissue macrophages, which are transformed toward overproduction of enzymes that degrade cartilage and bone and cytokines that promote immune cell infiltration. Recent studies have shown metabolic changes in both FLS and macrophages from RA patients, and these may be therapeutically targetable. However, because the origins and subset-specific functions of synoviocytes are poorly understood, and the signaling modules that control metabolic deviation in RA synovial cells are yet to be explored, significant additional research is needed to translate these findings to clinical application. Furthermore, in many inflamed tissues, different cell types can forge metabolic collaborations through solute carriers in their membranes to meet a high demand for energy or biomolecules. Such relationships are likely to exist in the synovium and have not been studied. Finally, it is not yet known whether metabolic change is a consequence of disease or whether primary changes to cellular metabolism might underlie or contribute to the pathogenesis of early-stage disease. In this review article, we collate what is known about metabolism in synovial tissue cells and highlight future directions of research in this area.

Indexed as

Arthritis, RheumatoidCartilageChronic DiseaseCytokinesFibroblastsHumansInflammationMacrophagesMetabolomeSynovial MembraneSynoviocytesCytokines

Identifiers

PMID29579371
PMCPMC6019623
OpenAlexW2789246385

What OpenQuestion holds

Textmetadata
LicenceTDM
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.