Evidence map›Paper›PMID 40592720›Full record

ArticleRMD open2025

Shivakumar R Veerabhadraiah, Derek J Matheson, Matthew Honeggar, Collin Aslor, Antonio C Zelada, Chris Stubben, Gregory J Stoddard, Nikolas H Kazmers, David J Grunwald, Michael J Jurynec

Abstract read
In one paragraph

Article in RMD open, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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.

Shivakumar R VeerabhadraiahDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA.
Derek J MathesonDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA.
Matthew HoneggarDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA.
Collin AslorDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA.
Antonio C ZeladaDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA.
Chris StubbenHuntsman Cancer Institute Cancer Hospital, Salt Lake, Utah, USA.
Gregory J StoddardDivision of Epidemiology, University of Utah Health, Salt Lake, Utah, USA.
Nikolas H KazmersDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA.
David J GrunwaldDepartment of Human Genetics, University of Utah Health, Salt Lake, Utah, USA.
Michael J JurynecDepartment of Orthopaedics, University of Utah Health, Salt Lake, Utah, USA mjurynec@genetics.utah.edu.ORCID 0000-0003-2702-9164

Funding

UTAH REGIONAL CANCER CENTERP30CA042014 · NCI · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI Jared P Rutter · 1986 to 2026
$72.6M
CTSA UM1 Program at University of UtahUM1TR004409 · NCATS · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI RACHEL HESS, Jennifer Juhl Majersik · 2023 to 2026
$21.9M
Contribution of the NOD/RIPK2 signaling pathway to osteoarthritis susceptibilityR01AR082973 · NIAMS · UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAH · PI MICHAEL J JURYNEC · 2024 to 2026
$1.7M
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 UM1 TR004409NCI NIH HHS P30 CA042014NIAMS NIH HHS R01 AR082973NIA NIH HHS R21 AG063534
6 · The paper itself

Abstract

objectiveChondrocytes of the synovial joint sense and respond to changes in osmolarity to maintain joint homeostasis. We hypothesised that an abnormal response to osmotic stress is a contributing factor to loss of joint homeostasis and the development of osteoarthritis (OA). Our goal was to identify whether genetic variants affecting the response to osmotic stress were associated with susceptibility to OA.

methodsGenomic analysis of independent families with dominant inheritance of OA revealed novel

resultsWe identified novel coding variants of

conclusionsOur data indicate elevated WNK2 signalling is associated with heightened susceptibility to OA. We hypothesise the synergistic effects of hyperosmotic stress and high WNK2 activity promote the development of OA.

Indexed as

ChondrocytesOsmotic PressureOsteoarthritisProtein Serine-Threonine KinasesAdultAgedAnimalsFemaleGenetic Predisposition to DiseaseHumansMaleMiceMiddle AgedPedigreeProtein Serine-Threonine KinasesChondrocytesInflammationOsteoarthritisPolymorphism, Genetic

Identifiers

PMID40592720
PMCPMC12215121

What OpenQuestion holds

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LicenceCC BY
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.