Evidence map›Paper›PMID 19898488›Full record

ArticleNature medicine2009

Synovial fibroblasts spread rheumatoid arthritis to unaffected joints.

Stephanie Lefèvre, Anette Knedla, Christoph Tennie, Andreas Kampmann, Christina Wunrau, Robert Dinser, Adelheid Korb, Eva-Maria Schnäker, Ingo H Tarner, Paul D Robbins and 8 more

Registry-linked trialAbstract read
In one paragraph

Article in Nature medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04092244 (CTHRC1 as a New Biomarker in Diagnosis of Rheumatoid Arthritis and Its Role in Seronegative Patients.), which is not on this map. Cited by 298 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
298citing papers in PubMed, 3 pooled it
23.0field-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.

NCT04092244 unknown statusnot on this mapstarted 2020, after this paper: background citation

CTHRC1 as a New Biomarker in Diagnosis of Rheumatoid Arthritis and Its Role in Seronegative Patients.

TypeobservationalSponsorAssiut UniversityRan2020 to 2021Enrolled90ConditionsRheumatoid ArthritisArmsCTHRC1 biomarker
3 · Its place in the literature

Who cites it

298 citing papers in PubMed, 3 syntheses or guidelines pooled it, 698 citations in OpenAlex.

  1. Pooled it
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  12. Charge-reversal proteolysis polymers enable tissue-specific STING degradation in rheumatoid arthritis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
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  19. Galectin-9 inhibition of the MIF-CD74/CD44 pathway suppresses chronic arthritis.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  20. Review

238 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

18 authors at 8 institutions in 3 countries.

Stephanie LefèvreDepartment of Internal Medicine and Rheumatology, Justus-Liebig-University Giessen, Kerckhoff-Clinic, Bad Nauheim, Germany.
Anette Knedla
Christoph Tennie
Andreas Kampmann
Christina Wunrau
Robert Dinser
Adelheid Korb
Eva-Maria Schnäker
Ingo H Tarner
Paul D Robbins
Christopher H Evans
Henning Stürz
Jürgen Steinmeyer
Steffen Gay
Jürgen Schölmerich
Thomas Pap
Ulf Müller-Ladner
Elena Neumann
Kerckhoff Klinik · DEUniversity Hospital Münster · DEUniversitätsklinikum Gießen und Marburg · DEUniversity of Giessen · DEHarvard University · USSwiss Integrative Center for Human Health · CHUniversity of Pittsburgh · USUniversity of Regensburg · DE

Funding

LMP and Bone HealingR01AR051456 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROBBINS, PAUL D. · 2008 to 2012
$1.7M
NIAMS NIH HHS R01 AR051456
6 · The paper itself

Abstract

Active rheumatoid arthritis originates from few joints but subsequently affects the majority of joints. Thus far, the pathways of the progression of the disease are largely unknown. As rheumatoid arthritis synovial fibroblasts (RASFs) which can be found in RA synovium are key players in joint destruction and are able to migrate in vitro, we evaluated the potential of RASFs to spread the disease in vivo. To simulate the primary joint of origin, we implanted healthy human cartilage together with RASFs subcutaneously into severe combined immunodeficient (SCID) mice. At the contralateral flank, we implanted healthy cartilage without cells. RASFs showed an active movement to the naive cartilage via the vasculature independent of the site of application of RASFs into the SCID mouse, leading to a marked destruction of the target cartilage. These findings support the hypothesis that the characteristic clinical phenomenon of destructive arthritis spreading between joints is mediated, at least in part, by the transmigration of activated RASFs.

Indexed as

AnimalsArthritis, RheumatoidCartilageCell AdhesionCell MovementDisease ProgressionExtracellular MatrixFibroblastsHumansMiceMice, SCIDSynovial MembraneTransplantation, Heterologous

Identifiers

PMID19898488
PMCPMC3678354
OpenAlexW1997131908

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.