Evidence map›Paper›PMID 33395574›Full record

ArticleOsteoarthritis and cartilage2021

Activation of TRPV4 by mechanical, osmotic or pharmaceutical stimulation is anti-inflammatory blocking IL-1β mediated articular cartilage matrix destruction.

S Fu, H Meng, S Inamdar, B Das, H Gupta, W Wang, C L Thompson, M M Knight

Open access · hybridAbstract read
In one paragraph

Article in Osteoarthritis and cartilage, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

49 citing papers in PubMed, 70 citations in OpenAlex.

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  13. Ion channels as therapeutic targets in osteoarthritis.Trends in pharmacological sciences · 2025
    Review
  14. [Effect of mechanical stimuli on physicochemical properties of joint fluid in osteoarthritis].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2025
    Review
  15. RMD open · 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

8 authors at 1 institution in 2 countries.

S FuCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: s.fu@qmul.ac.uk.
H MengCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: Huan.meng@qmul.ac.uk.
S InamdarCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: s.r.inamdar@qmul.ac.uk.
B DasCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK.
H GuptaCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: h.gupta@qmul.ac.uk.
W WangCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: Wen.wang@qmul.ac.uk.
C L ThompsonCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: Clare.l.thompson@qmul.ac.uk.
M M KnightCentre for Predictive In Vitro Models, School of Engineering and Materials Science, Queen Mary University of London, UK. Electronic address: m.m.knight@qmul.ac.uk.
Queen Mary University of London · GB

Funding

Biotechnology and Biological Sciences Research Council BB/R003610/1Medical Research Council MR/L002876/1
6 · The paper itself

Abstract

objectiveCartilage health is maintained in response to a range of mechanical stimuli including compressive, shear and tensile strains and associated alterations in osmolality. The osmotic-sensitive ion channel Transient Receptor Potential Vanilloid 4 (TRPV4) is required for mechanotransduction. Mechanical stimuli inhibit interleukin-1β (IL-1β) mediated inflammatory signalling, however the mechanism is unclear. This study aims to clarify the role of TRPV4 in this response.

designTRPV4 activity was modulated glycogen synthase kinase (GSK205 antagonist or GSK1016790 A (GSK101) agonist) in articular chondrocytes and cartilage explants in the presence or absence of IL-1β, mechanical (10% cyclic tensile strain (CTS), 0.33 Hz, 24hrs) or osmotic loading (200mOsm, 24hrs). Nitric oxide (NO), prostaglandin E

resultsIn isolated chondrocytes, mechanical loading inhibited IL-1β mediated NO and PGE

conclusionMechanical, osmotic or pharmaceutical activation of TRPV4 regulates HDAC6-dependent modulation of ciliary tubulin and is anti-inflammatory. This study reveals for the first time, the potential of TRPV4 manipulation as a novel therapeutic mechanism to supress pro-inflammatory signalling and cartilage degradation.

Indexed as

AnimalsBiomechanical PhenomenaCartilage, ArticularCattleChondrocytesDinoprostoneGlycosaminoglycansHistone Deacetylase 6InflammationInterleukin-1betaLeucineMechanotransduction, CellularNitric OxideOsmotic PressureStress, MechanicalSulfonamidesA73025DinoprostoneGlycosaminoglycansHistone Deacetylase 6Interleukin-1betaLeucineN-(1-((4-(2-(((2,4-dichlorophenyl)sulfonyl)amino)-3-hydroxypropanoyl)-1-piperazinyl)carbonyl)-3-methylbutyl)-1-benzothiophene-2-carboxamideNitric OxideSulfonamidesTRPV Cation ChannelsCartilageCiliaHypo-osmolarityIL-1βMechanotransductionTRPV4

Identifiers

PMID33395574
PMCPMC7799379
OpenAlexW3117439016

What OpenQuestion holds

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LicenceCC BY
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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.