Evidence map›Paper›PMID 32418287›Full record

ArticleArthritis & rheumatology (Hoboken, N.J.)2020

Deletion of JNK Enhances Senescence in Joint Tissues and Increases the Severity of Age-Related Osteoarthritis in Mice.

Richard F Loeser, Kathryn L Kelley, Alexandra Armstrong, John A Collins, Brian O Diekman, Cathy S Carlson

Open access · greenAbstract read
In one paragraph

Article in Arthritis & rheumatology (Hoboken, N.J.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-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

24 citing papers in PubMed, 41 citations in OpenAlex.

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  6. The role of JNK signaling pathway in organ fibrosis.Journal of advanced research · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

Richard F LoeserUniversity of North Carolina School of Medicine, Chapel Hill.ORCID 0000-0003-2832-6144
Kathryn L KelleyUniversity of North Carolina School of Medicine, Chapel Hill.
Alexandra ArmstrongUniversity of Minnesota College of Veterinary Medicine, St. Paul.
John A CollinsUniversity of North Carolina School of Medicine, Chapel Hill.
Brian O DiekmanUniversity of North Carolina School of Medicine, Chapel Hill, and North Carolina State University, Raleigh.
Cathy S CarlsonUniversity of Minnesota College of Veterinary Medicine, St. Paul.
University of North Carolina at Chapel Hill · USUniversity of Minnesota · USNorth Carolina State University · US

Funding

Oxidative Stress and the Development of OsteoarthritisR01AG044034 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI RICHARD F LOESER · 2012 to 2026
$5.7M
Integrin Function in CartilageR37AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2012 to 2021
$4.1M
Musculoskeletal Training GrantT32AR050938 · NIAMS · UNIVERSITY OF MINNESOTA TWIN CITIES · PI CLOHISY, DENIS R · 2004 to 2020
$3.0M
Integrin Function in CartilageR01AR049003 · NIAMS · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI LOESER, RICHARD F · 2002 to 2011
$2.8M
NIAMS NIH HHS R01 AR049003NIAMS NIH HHS R37 AR049003NIAMS NIH HHS T32 AR050938NIA NIH HHS R01 AG044034
6 · The paper itself

Abstract

objectiveTo determine the role of JNK signaling in the development of osteoarthritis (OA) induced by joint injury or aging in mice.

methodsIn the joint injury model, 12-week-old wild-type control, JNK1

resultsThere were no differences after DMM surgery between the wild-type and the JNK-knockout mouse groups in articular cartilage structure, toluidine blue, or osteophyte scores or in MMP-13 production in explants. All 3 knockout mouse groups had increased subchondral bone thickness and area of cartilage necrosis compared to wild-type mice. Aged JNK-knockout mice had significantly worse articular cartilage structure scores compared to the aged wild-type control mice (mean ± SD 52 ± 24 in JNK1

conclusionJNK1 and JNK2 are not required for the development of OA in the mouse DMM model. Deletion of JNK1 or JNK2 is associated with more severe age-related OA and increased cell senescence, suggesting that JNK may act as a negative regulator of senescence in the joint.

Indexed as

AgingAnimalsCartilage, ArticularCellular SenescenceChondrocytesDisease Models, AnimalKnee JointMatrix Metalloproteinase 13MiceMice, KnockoutMitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9OsteoarthritisSeverity of Illness IndexMatrix Metalloproteinase 13Mitogen-Activated Protein Kinase 8Mitogen-Activated Protein Kinase 9

Identifiers

PMID32418287
PMCPMC7669715
OpenAlexW3025654853

What Socratic 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 Socratic graph.