Evidence map›Paper›PMID 36810185›Full record

ArticleRMD open2023

NADPH oxidase 4 deficiency attenuates experimental osteoarthritis in mice.

Félix Renaudin, Karim Oudina, Maude Gerbaix, Manon McGilligan Subilia, Joris Paccaud, Vincent Jaquet, Karl-Heinz Krause, Serge Ferrari, Thomas Laumonier, Didier Hannouche

Open access · goldAbstract read
In one paragraph

Article in RMD open, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

10 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
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

10 authors at 1 institution in 2 countries.

Félix RenaudinDepartment of Cell Physiology and Metabolism, Université de Genève Faculté de médecine, Geneve, Switzerland.ORCID 0000-0002-5712-582X
Karim OudinaDepartment of Cell Physiology and Metabolism, Université de Genève Faculté de médecine, Geneve, Switzerland.
Maude GerbaixService of Bone Diseases, Department of Medicine, Geneva University Hospitals, Geneve, Switzerland.
Manon McGilligan SubiliaDepartment of Cell Physiology and Metabolism, Université de Genève Faculté de médecine, Geneve, Switzerland.
Joris PaccaudDepartment of Cell Physiology and Metabolism, Université de Genève Faculté de médecine, Geneve, Switzerland.
Vincent JaquetDepartment of Pathology and Immunology, Université de Genève Faculté de médecine, Geneve, Switzerland.
Karl-Heinz KrauseDepartment of Pathology and Immunology, Université de Genève Faculté de médecine, Geneve, Switzerland.
Serge FerrariService of Bone Diseases, Department of Medicine, Geneva University Hospitals, Geneve, Switzerland.
Thomas LaumonierDepartment of Cell Physiology and Metabolism, Université de Genève Faculté de médecine, Geneve, Switzerland.
Didier HannoucheDepartment of Cell Physiology and Metabolism, Université de Genève Faculté de médecine, Geneve, Switzerland Didier.Hannouche@hcuge.ch.
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveLow-grade inflammation plays a pivotal role in osteoarthritis (OA) through exposure to reactive oxygen species (ROS). In chondrocytes, NADPH oxidase 4 (NOX4) is one of the major ROS producers. In this study, we evaluated the role of NOX4 on joint homoeostasis after destabilisation of the medial meniscus (DMM) in mice.

methodsExperimental OA was simulated on cartilage explants using interleukin-1β (IL-1β) and induced by DMM in wild-type (WT) and NOX4 knockout (NOX4

resultsWhole body NOX4 deletion attenuated experimental OA in mice, with a significant reduction of the OARSI score at 8 weeks. DMM increased total subchondral bone plate (SB.Th), epiphysial trabecular thicknesses (Tb.Th) and bone volume fraction (BV/TV) in both NOX4

conclusionNOX4 deficiency restores cartilage homoeostasis, inhibits oxidative stress, inflammation and delays OA progression after DMM in mice. These findings suggest that NOX4 represent a potential target to counteract for OA treatment.

Indexed as

NADPH Oxidase 4OsteoarthritisAnimalsDisease Models, AnimalInflammationMiceMice, KnockoutReactive Oxygen SpeciesNADPH Oxidase 4Nox4 protein, mouseReactive Oxygen SpeciesCytokinesInflammationOsteoarthritis

Identifiers

PMID36810185
PMCPMC9945017
OpenAlexW4321452042

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.