Evidence map›Paper›PMID 32273577›Full record

ReviewNature reviews. Rheumatology2020

Interplay between genetics and epigenetics in osteoarthritis.

Sarah J Rice, Frank Beier, David A Young, John Loughlin

Abstract readComparative StudyReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Rheumatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 2 pooled it
9.3field-weighted citation impact, top 1% 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

102 citing papers in PubMed, 2 syntheses or guidelines pooled it, 161 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. The complexity of pain in osteoarthritis.Nature reviews. Rheumatology · 2026
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Osteoarthritis as a systemic disease.Nature reviews. Rheumatology · 2026
    Review
  16. Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026
    Review
  17. Review
  18. Article
  19. Article
  20. Article

42 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 2 countries.

Sarah J RiceBiosciences Institute, Newcastle University, Newcastle upon Tyne, UK.
Frank BeierDepartment of Physiology and Pharmacology, The University of Western Ontario, London, ON, Canada.ORCID http://orcid.org/0000-0002-8505-7537
David A YoungBiosciences Institute, Newcastle University, Newcastle upon Tyne, UK.ORCID http://orcid.org/0000-0002-7078-6745
John LoughlinBiosciences Institute, Newcastle University, Newcastle upon Tyne, UK. john.loughlin@ncl.ac.uk.ORCID http://orcid.org/0000-0003-2018-3361
Newcastle University · GBWestern University · CA

Funding

CIHR 332438Medical Research Council MR/P020941/1Medical Research Council MR/R502182/1The Dunhill Medical Trust R476/0516Versus Arthritis 20771
6 · The paper itself

Abstract

Research into the molecular genetics of osteoarthritis (OA) has been substantially bolstered in the past few years by the implementation of powerful genome-wide scans that have revealed a large number of novel risk loci associated with the disease. This refreshing wave of discovery has occurred concurrently with epigenetic studies of joint tissues that have examined DNA methylation, histone modifications and regulatory RNAs. These epigenetic analyses have involved investigations of joint development, homeostasis and disease and have used both human samples and animal models. What has become apparent from a comparison of these two complementary approaches is that many OA genetic risk signals interact with, map to or correlate with epigenetic mediators. This discovery implies that epigenetic mechanisms, and their effect on gene expression, are a major conduit through which OA genetic risk polymorphisms exert their functional effects. This observation is particularly exciting as it provides mechanistic insight into OA susceptibility. Furthermore, this knowledge reveals avenues for attenuating the negative effect of risk-conferring alleles by exposing the epigenome as an exploitable target for therapeutic intervention in OA.

Indexed as

AllelesAnimalsChondrocytesDNA MethylationEpigenomicsGene ExpressionGenome-Wide Association StudyHistone CodeHomeostasisHumansJointsMiceModels, AnimalOsteoarthritisPolymorphism, Single NucleotideRegulatory Sequences, Ribonucleic AcidRegulatory Sequences, Ribonucleic Acid

Identifiers

PMID32273577
OpenAlexW3015291397

What OpenQuestion holds

Textmetadata
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.