Evidence map›Paper›PMID 39331223›Full record

ArticleMolecular biology reports2024

Disuse atrophy of articular cartilage can be restored by mechanical reloading in mice.

Masato Nomura, Hideki Moriyama, Yoshio Wakimoto, Yasushi Miura

Erratum issuedAbstract read
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Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

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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

3 citing papers in PubMed.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Masato NomuraDepartment of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Tomogaoka 7-10-2, Suma-ku, Kobe, Hyogo, 654-0142, Japan. cunorimousiraty@gmail.com.
Hideki MoriyamaDepartment of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Tomogaoka 7-10-2, Suma-ku, Kobe, Hyogo, 654-0142, Japan.
Yoshio WakimotoDepartment of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Tomogaoka 7-10-2, Suma-ku, Kobe, Hyogo, 654-0142, Japan.
Yasushi MiuraDepartment of Rehabilitation Science, Kobe University Graduate School of Health Sciences, Tomogaoka 7-10-2, Suma-ku, Kobe, Hyogo, 654-0142, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundModerate mechanical stress generated by normal joint loading and movements helps maintain the health of articular cartilage. Despite growing interest in the pathogenesis of cartilage degeneration caused by reduced mechanical stress, its reversibility by mechanical reloading is less understood. This study aimed to investigate the response of articular cartilage exposed to mechanical reloading after unloading in vivo and in vitro. METHODS AND

resultsDisuse atrophy was induced in the knee joint cartilage of adult mice through hindlimb unloading by tail suspension. For in vivo experiments, mice were subjected to reloading with or without daily exercise intervention or surgical destabilization of the knee joint. Microcomputed tomography and histomorphometric analyses were performed on the harvested knee joints. Matrix loss and thinning of articular cartilage due to unloading were fully or partially restored by reloading, and exercise intervention enhanced the restoration. Subchondral bone density decreased by unloading and increased to above-normal levels by reloading. The severity of cartilage damage caused by joint instability was not different even with prior non-weight bearing. For in vitro experiments, articular chondrocytes isolated from the healthy or unloaded joints of the mice were embedded in agarose gel. After dynamic compression loading, the expression levels of anabolic (Sox9, Col2a1, and Acan) and catabolic (Mmp13 and Adamts5) factors of cartilage were analyzed. In chondrocytes isolated from the unloaded joints, similar to those from healthy joints, dynamic compression increased the expression of anabolic factors but suppressed the expression of catabolic factors.

conclusionThe results of this study indicate that the morphological changes in articular cartilage exposed to mechanical unloading may be restored in response to mechanical reloading by shifting extracellular matrix metabolism in chondrocytes to anabolism.

Indexed as

ADAMTS5 ProteinCartilage, ArticularChondrocytesHindlimb SuspensionStress, MechanicalAggrecansAnimalsAtrophyCollagen Type IIDisease Models, AnimalKnee JointMaleMatrix Metalloproteinase 13MiceMice, Inbred C57BLPhysical Conditioning, AnimalAcan protein, mouseADAMTS5 ProteinAdamts5 protein, mouseAggrecansCol2a1 protein, mouseCollagen Type IIMatrix Metalloproteinase 13Mmp13 protein, mouseSox9 protein, mouseSOX9 Transcription FactorArticular cartilageDisuse atrophyMechanical loadingReversibilitySubchondral bone

Identifiers

PMID39331223
PMCPMC11436453

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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.