Evidence map›Paper›PMID 35732460›Full record

ArticleAnnals of the rheumatic diseases2022

NOD/RIPK2 signalling pathway contributes to osteoarthritis susceptibility.

Michael J Jurynec, Catherine M Gavile, Matthew Honeggar, Ying Ma, Shivakumar R Veerabhadraiah, Kendra A Novak, Kazuyuki Hoshijima, Nikolas H Kazmers, David J Grunwald

Open access · greenAbstract read
In one paragraph

Article in Annals of the rheumatic diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
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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

9 authors at 1 institution in 1 country.

Michael J JurynecDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA mjurynec@genetics.utah.edu.ORCID http://orcid.org/0000-0003-2702-9164
Catherine M GavileDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA.
Matthew HoneggarDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA.
Ying MaDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA.
Shivakumar R VeerabhadraiahDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA.
Kendra A NovakDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA.
Kazuyuki HoshijimaDepartment of Human Genetics, University of Utah Health, Salt Lake City, Utah, USA.
Nikolas H KazmersDepartment of Orthopaedics, University of Utah Health, Salt Lake City, Utah, USA.
David J GrunwaldDepartment of Human Genetics, University of Utah Health, Salt Lake City, Utah, USA.
University of Utah · US

Funding

Utah Center for Clinical and Translational ScienceUL1TR002538 · NCATS · UNIVERSITY OF UTAH · PI HESS, RACHEL, MAJERSIK, JENNIFER JUHL · 2018 to 2022
$26.0M
Establishing a new genetic mouse model of osteoarthritisR21AG063534 · NIA · UNIVERSITY OF UTAH · PI GRUNWALD, DAVID J., JURYNEC, MICHAEL J · 2020 to 2021
$419k
NCATS NIH HHS UL1 TR002538NIA NIH HHS R21 AG063534
6 · The paper itself

Abstract

objectivesHow inflammatory signalling contributes to osteoarthritis (OA) susceptibility is undetermined. An allele encoding a hyperactive form of the Receptor Interacting Protein Kinase 2 (RIPK2) proinflammatory signalling intermediate has been associated with familial OA. To test whether altered nucleotide-binding oligomerisation domain (NOD)/RIPK2 pathway activity causes heightened OA susceptibility, we investigated whether variants affecting additional pathway components are associated with familial OA. To determine whether the

methodsGenomic analysis of 150 independent families with dominant inheritance of OA affecting diverse joints was used to identify coding variants that segregated strictly with occurrence of OA. Genome editing was used to introduce the OA-associated

resultsWe identified six novel variants affecting components of the NOD/RIPK2 inflammatory signalling pathway that are associated with familial OA affecting the hand, shoulder or foot. The

conclusionsTwo types of data support the hypothesis that altered NOD/RIPK2 signalling confers susceptibility to OA.

Indexed as

OsteoarthritisAllelesAnimalsCytokinesInflammationMiceReceptor-Interacting Protein Serine-Threonine Kinase 2Signal TransductionCytokinesReceptor-Interacting Protein Serine-Threonine Kinase 2Ripk2 protein, mousearthritis, experimentalinflammationosteoarthritispolymorphism, genetic

Identifiers

PMID35732460
PMCPMC9474725
OpenAlexW4283275222

What OpenQuestion holds

Textmetadata
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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.