Evidence map›Paper›PMID 34608249›Full record

ArticleScientific reports2021

BMP7 reduces the fibrocartilage chondrocyte phenotype.

Ellen G J Ripmeester, Marjolein M J Caron, Guus G H van den Akker, Jessica Steijns, Don A M Surtel, Andy Cremers, Laura C W Peeters, Lodewijk W van Rhijn, Tim J M Welting

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
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  10. DNA methylation of bone morphogenetic protein 7 in leukocytes as a possible biomarker for hand osteoarthritis: A pilot study.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025
    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 2 institutions in 2 countries.

Ellen G J RipmeesterLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Marjolein M J CaronLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands. marjolein.caron@maastrichtuniversity.nl.
Guus G H van den AkkerLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Jessica SteijnsLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Don A M SurtelLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Andy CremersLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Laura C W PeetersLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Lodewijk W van RhijnLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Tim J M WeltingLaboratory for Experimental Orthopedics, Department of Orthopedic Surgery, Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, The Netherlands.
Maastricht University · NLUniversity Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The fibrocartilage chondrocyte phenotype has been recognized to attribute to osteoarthritis (OA) development. These chondrocytes express genes related to unfavorable OA outcomes, emphasizing its importance in OA pathology. BMP7 is being explored as a potential disease-modifying molecule and attenuates the chondrocyte hypertrophic phenotype. On the other hand, BMP7 has been demonstrated to relieve organ fibrosis by counteracting the pro-fibrotic TGFβ-Smad3-PAI1 axis and increasing MMP2-mediated Collagen type I turnover. Whether BMP7 has anti-fibrotic properties in chondrocytes is unknown. Human OA articular chondrocytes (HACs) were isolated from end-stage OA femoral cartilage (total knee arthroplasty; n = 18 individual donors). SW1353 cells and OA HACs were exposed to 1 nM BMP7 for 24 h, after which gene expression of fibrosis-related genes and fibrosis-mediating factors was determined by RT-qPCR. In SW1353, Collagen type I protein levels were determined by immunocytochemistry and western blotting. PAI1 and MMP2 protein levels and activity were measured with an ELISA and activity assays, respectively. MMP2 activity was inhibited with the selective MMP-2 inhibitor OA-Hy. SMAD3 activity was determined by a (CAGA)

Indexed as

BiomarkersBone Morphogenetic Protein 7Cartilage, ArticularCells, CulturedChondrocytesDisease SusceptibilityEnzyme ActivationFibrocartilageGene ExpressionHumansImmunohistochemistryMatrix Metalloproteinase 2OsteoarthritisPhenotypeSignal TransductionBiomarkersBMP7 protein, humanBone Morphogenetic Protein 7Matrix Metalloproteinase 2MMP2 protein, human

Identifiers

PMID34608249
PMCPMC8490443
OpenAlexW3201880945

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.