Evidence map›Paper›PMID 26219087›Full record

ArticleScientific reports2015

Human xylosyltransferases--mediators of arthrofibrosis? New pathomechanistic insights into arthrofibrotic remodeling after knee replacement therapy.

Isabel Faust, Philipp Traut, Frank Nolting, Jan Petschallies, Elena Neumann, Elke Kunisch, Joachim Kuhn, Cornelius Knabbe, Doris Hendig

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  4. Observational
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  8. [Histopathological diagnostics of arthrofibrosis].Unfallchirurgie (Heidelberg, Germany) · 2022
    Review
  9. Review
  10. [Surgical treatment of arthrofibrosis of the knee joint].Unfallchirurgie (Heidelberg, Germany) · 2022
    Review
  11. Article
  12. Article
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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

9 authors at 4 institutions in 1 country.

Isabel FaustInstitut für Laboratoriums- und Transfusionsmedizin, Herz- und Diabeteszentrum Nordrhein-Westfalen, Universitätsklinik der Ruhr-Universität Bochum, Bad Oeynhausen, Germany.
Philipp TrautKlinik am Rosengarten, Bad Oeynhausen, Germany.
Frank NoltingKlinik am Rosengarten, Bad Oeynhausen, Germany.
Jan PetschalliesOrthopaedicum Hannover, Zentrum für orthopädische Chirurgie, Hannover, Germany.
Elena NeumannJustus-Liebig Universität Gießen, Internal Medicine and Rheumatology, Kerckhoff-Klinik Bad Nauheim, Bad Nauheim, Germany.
Elke KunischUniversitätsklinikum Jena, Rudolf-Elle Waldkrankenhaus Eisenberg, Eisenberg, Germany.
Joachim KuhnInstitut für Laboratoriums- und Transfusionsmedizin, Herz- und Diabeteszentrum Nordrhein-Westfalen, Universitätsklinik der Ruhr-Universität Bochum, Bad Oeynhausen, Germany.
Cornelius KnabbeInstitut für Laboratoriums- und Transfusionsmedizin, Herz- und Diabeteszentrum Nordrhein-Westfalen, Universitätsklinik der Ruhr-Universität Bochum, Bad Oeynhausen, Germany.
Doris HendigInstitut für Laboratoriums- und Transfusionsmedizin, Herz- und Diabeteszentrum Nordrhein-Westfalen, Universitätsklinik der Ruhr-Universität Bochum, Bad Oeynhausen, Germany.
Heart and Diabetes Center North Rhine-Westphalia · DEKlinik Bad Oexen · DEJena University Hospital · DEUniversity of Giessen · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Total knee replacement (TKR) is a common therapeutic option to restore joint functionality in chronic inflammatory joint diseases. Subsequent arthrofibrotic remodeling occurs in 10%, but the underlying pathomechanisms remain unclear. We evaluated the association of xylosyltransferases (XT), fibrotic mediators catalyzing glycosaminoglycan biosynthesis, leading to arthrofibrosis as well as the feasibility of using serum XT activity as a diagnostic marker. For this purpose, synovial fibroblasts (SF) were isolated from arthrofibrotic and control synovial biopsies. Basal α-smooth muscle actin expression revealed a high fibroblast-myofibroblast transition rate in arthrofibrotic fibroblasts. Fibrotic remodeling marked by enhanced XT activity, α-SMA protein expression as well as xylosyltransferase-I, collagen type III-alpha-1 and ACTA2 mRNA expression was stronger in arthrofibrotic than in control fibroblasts treated with transforming growth factor-β1 (TGF-β1). Otherwise, no differences between serum levels of XT-I activity or common fibrosis markers (galectin-3 and growth differentiation factor-15 levels (GDF-15)) were found between 95 patients with arthrofibrosis and 132 controls after TKR. In summary, XT-I was initially investigated as a key cellular mediator of arthrofibrosis and a target for therapeutic intervention. However, the blood-synovial-barrier makes arthrofibrotic molecular changes undetectable in serum. Future studies on monitoring or preventing arthrofibrotic remodeling should therefore rely on local instead of systemic parameters.

Indexed as

ActinsAgedArthroplasty, Replacement, KneeCase-Control StudiesEnzyme ActivationExtracellular MatrixFibroblastsFibrosisGalectin 3Gene Expression RegulationGrowth Differentiation Factor 15HumansJoint DiseasesKnee JointMiddle AgedPentosyltransferasesACTA2 protein, humanActinsGalectin 3Growth Differentiation Factor 15PentosyltransferasesTransforming Growth Factor beta1UDP Xylose-Protein Xylosyltransferase

Identifiers

PMID26219087
PMCPMC4517395
OpenAlexW2236679049

What OpenQuestion holds

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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.