Evidence map›Paper›PMID 34829531›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Nik N L Kruisbergen, Irene Di Ceglie, Yvonne van Gemert, Birgitte Walgreen, Monique M A Helsen, Annet W Slöetjes, Marije I Koenders, Fons A J van de Loo, Johannes Roth, Thomas Vogl and 4 more

Abstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
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

14 authors.

Nik N L KruisbergenExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Irene Di CeglieExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Yvonne van GemertExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Birgitte WalgreenExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Monique M A HelsenExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Annet W SlöetjesExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Marije I KoendersExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Fons A J van de LooExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Johannes RothInstitute of Immunology, University of Münster, 48149 Muenster, Germany.
Thomas VoglInstitute of Immunology, University of Münster, 48149 Muenster, Germany.
Peter M van der KraanExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Arjen B BlomExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Peter L E M van LentExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.
Martijn H J van den BoschExperimental Rheumatology, Department of Rheumatology, Radboud University Medical Center, 6525GA Nijmegen, The Netherlands.ORCID 0000-0001-8074-826X

Funding

Reumafonds 16-1-402
6 · The paper itself

Abstract

Osteoarthritis (OA) is a destructive disease of the joint with age and obesity being its most important risk factors. Around 50% of OA patients suffer from inflammation of the synovial joint capsule, which is characterized by increased abundance and activation of synovial macrophages that produce reactive oxygen species (ROS) via NADPH-oxidase 2 (NOX2). Both ROS and high blood levels of low-density lipoprotein (LDL) are implicated in OA pathophysiology, which may interact to form oxidized LDL (oxLDL) and thereby promote disease. Therefore, targeting NOX2 could be a viable treatment strategy for OA. Collagenase-induced OA (CiOA) was used to compare pathology between wild-type (WT) and Nox2 knockout (

Indexed as

low-density lipoproteinMacrophagesNOX2osteoarthritisROS

Identifiers

PMID34829531
PMCPMC8614813

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.