Evidence map›Paper›PMID 26511510›Full record

ArticleScience translational medicine2015

Inflammation activation and resolution in human tendon disease.

Stephanie G Dakin, Fernando O Martinez, Clarence Yapp, Graham Wells, Udo Oppermann, Benjamin J F Dean, Richard D J Smith, Kim Wheway, Bridget Watkins, Lucy Roche and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Science translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
140citing papers in PubMed, 5 pooled it
14.7field-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

140 citing papers in PubMed, 5 syntheses or guidelines pooled it, 257 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Article
  8. Grafts in tendon repair.Materials today. Bio · 2026
    Review
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80 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

11 authors at 1 institution in 1 country.

Stephanie G DakinNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Fernando O MartinezNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK.
Clarence YappStructural Genomics Consortium, University of Oxford, Old Road Campus, Headington OX3 7DQ, UK.
Graham WellsNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK.
Udo OppermannNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. Structural Genomics Consortium, University of Oxford, Old Road Campus, Headington OX3 7DQ, UK.
Benjamin J F DeanNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Richard D J SmithNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Kim WhewayNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Bridget WatkinsNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Lucy RocheNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Andrew J CarrNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Botnar Research Centre, University of Oxford, Nuffield Orthopaedic Centre, Headington OX3 7LD, UK. NIHR Oxford Biomedical Research Unit, Botnar Research Centre, University of Oxford, Oxford OX3 7LD, UK.
Nuffield Orthopaedic Centre · GB

Funding

Arthritis Research UK 20506CIHRVersus Arthritis 20506Versus Arthritis 20522Wellcome Trust 106169
6 · The paper itself

Abstract

Improved understanding of the role of inflammation in tendon disease is required to facilitate therapeutic target discovery. We studied supraspinatus tendons from patients experiencing pain before and after surgical subacromial decompression treatment. Tendons were classified as having early, intermediate, or advanced disease, and inflammation was characterized through activation of pathways mediated by interferon (IFN), nuclear factor κB (NF-κB), glucocorticoid receptor, and signal transducer and activator of transcription 6 (STAT-6). Inflammation signatures revealed expression of genes and proteins induced by IFN and NF-κB in early-stage disease and genes and proteins induced by STAT-6 and glucocorticoid receptor activation in advanced-stage disease. The proresolving proteins FPR2/ALX and ChemR23 were increased in early-stage disease compared to intermediate- to advanced-stage disease. Patients who were pain-free after treatment had tendons with increased expression of CD206 and ALOX15 mRNA compared to tendons from patients who continued to experience pain after treatment, suggesting that these genes and their pathways may moderate tendon pain. Stromal cells from diseased tendons cultured in vitro showed increased expression of NF-κB and IFN target genes after treatment with lipopolysaccharide or IFNγ compared to stromal cells derived from healthy tendons. We identified 15-epi lipoxin A4, a stable lipoxin isoform derived from aspirin treatment, as potentially beneficial in the resolution of tendon inflammation.

Indexed as

AdolescentAdultArachidonate 15-LipoxygenaseAspirinFemaleHumansImmunohistochemistryInflammationInterferon-gammaInterferonsIn Vitro TechniquesLectins, C-TypeLipopolysaccharidesLipoxinsMaleMannose-Binding LectinsALOX15 protein, humanArachidonate 15-LipoxygenaseAspirinCMKLR1 protein, humanFPR2 protein, humanInterferon-gammaInterferonsLectins, C-TypeLipopolysaccharideslipoxin A4LipoxinsMannose-Binding LectinsMannose ReceptorNF-kappa BReceptors, Cell SurfaceReceptors, ChemokineReceptors, Formyl PeptideReceptors, LipoxinSTAT6 Transcription Factor

Identifiers

PMID26511510
PMCPMC4883654
OpenAlexW2258281454

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.