Evidence map›Paper›PMID 26521740›Full record

ReviewOsteoarthritis and cartilage2015

Human genome-wide expression analysis reorients the study of inflammatory mediators and biomechanics in osteoarthritis.

J D Sandy, D D Chan, R L Trevino, M A Wimmer, A Plaas

Abstract readReview
In one paragraph

Review in Osteoarthritis and cartilage, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
4.3field-weighted citation impact, top 6% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  3. Review
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  5. Review
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  13. Suppression of murine osteoarthritis by 4-methylumbelliferone.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020
    Article
  14. Aging · 2020
    Article
  15. Development of a simple osteoarthritis model useful to predict in vitro the anti-hypertrophic action of drugs.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  16. Article
  17. 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

5 authors at 1 institution in 1 country.

J D SandyDepartment of Biochemistry, Rush University Medical Center, USA. Electronic address: jsandy44@gmail.com.
D D ChanSection of Rheumatology, Department of Internal Medicine, Rush University Medical Center, USA. Electronic address: deva_chan@rush.edu.
R L TrevinoDepartment of Anatomy and Cell Biology, Rush University Medical Center, USA. Electronic address: robert_trevino@rush.edu.
M A WimmerDepartment of Biochemistry, Rush University Medical Center, USA; Section of Rheumatology, Department of Internal Medicine, Rush University Medical Center, USA; Department of Orthopedic Surgery, Rush University Medical Center, USA. Electronic address: markus_a_wimmer@rush.edu.
A PlaasDepartment of Biochemistry, Rush University Medical Center, USA; Section of Rheumatology, Department of Internal Medicine, Rush University Medical Center, USA. Electronic address: anna_plaas@rush.edu.
Rush University Medical Center · US

Funding

Cartilage Degeneration and Repair By ADAMTSs and Hyaluronan Binding ProteinsR01AR057066 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI PLAAS, ANNA H. · 2011 to 2015
$1.7M
NIAMS NIH HHS R01 AR057066NIAMS NIH HHS R01-AR057066
6 · The paper itself

Abstract

A major objective of this article is to examine the research implications of recently available genome-wide expression profiles of cartilage from human osteoarthritis (OA) joints. We propose that, when viewed in the light of extensive earlier work, this novel data provides a unique opportunity to reorient the design of experimental systems toward clinical relevance. Specifically, in the area of cartilage explant biology, this will require a fresh evaluation of existing paradigms, so as to optimize the choices of tissue source, cytokine/growth factor/nutrient addition, and biomechanical environment for discovery. Within this context, we firstly discuss the literature on the nature and role of potential catabolic mediators in OA pathology, including data from human OA cartilage, animal models of OA, and ex vivo studies. Secondly, due to the number and breadth of studies on IL-1β in this area, a major focus of the article is a critical analysis of the design and interpretation of cartilage studies where IL-1β has been used as a model cytokine. Thirdly, the article provides a data-driven perspective (including genome-wide analysis of clinical samples, studies on mutant mice, and clinical trials), which concludes that IL-1β should be replaced by soluble mediators such as IL-17 or TGF-β1, which are much more likely to mimic the disease in OA model systems. We also discuss the evidence that changes in early OA can be attributed to the activity of such soluble mediators, whereas late-stage disease results more from a chronic biomechanical effect on the matrix and cells of the remaining cartilage and on other local mediator-secreting cells. Lastly, an updated protocol for in vitro studies with cartilage explants and chondrocytes (including the use of specific gene expression arrays) is provided to motivate more disease-relevant studies on the interplay of cytokines, growth factors, and biomechanics on cellular behavior.

Indexed as

Gene ExpressionGenome, HumanOsteoarthritisAnimalsBiomechanical PhenomenaCartilage, ArticularChondrocytesDNAHumansInflammation MediatorsDNAInflammation MediatorsBioinformaticsBiomechanicsCytokinesGrowth factorsInflammationOsteoarthritis

Identifiers

PMID26521740
PMCPMC4630670
OpenAlexW1854205368

What OpenQuestion holds

Textmetadata
LicenceTDM
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.