Evidence map›Paper›PMID 39448593›Full record

ArticleNature communications2024

IGF1 drives Wnt-induced joint damage and is a potential therapeutic target for osteoarthritis.

Ana Escribano-Núñez, Frederique M F Cornelis, Astrid De Roover, An Sermon, Frédéric Cailotto, Rik J Lories, Silvia Monteagudo

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing 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

17 citing papers in PubMed.

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  16. Wnt-induced IGF1 drives OA.Nature reviews. Rheumatology · 2025
    Article
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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

7 authors.

Ana Escribano-NúñezLaboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Centre, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.ORCID 0000-0002-4057-8400
Frederique M F CornelisLaboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Centre, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.ORCID 0000-0002-4144-5861
Astrid De RooverLaboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Centre, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.ORCID 0000-0003-0321-2896
An SermonDivision of Trauma Surgery, University Hospitals Leuven, Leuven, Belgium.ORCID 0000-0001-6295-9127
Frédéric CailottoCNRS-University of Lorraine, Molecular Engineering and Articular Physiopathology, Biopôle, University of Lorraine; Campus Biologie-Santé, Vandœuvre-Lès-Nancy, France.ORCID 0000-0002-4941-9238
Rik J Lories *Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Centre, Department of Development and Regeneration, KU Leuven, Leuven, Belgium.ORCID 0000-0002-5986-3092
Silvia Monteagudo *Laboratory of Tissue Homeostasis and Disease, Skeletal Biology and Engineering Research Centre, Department of Development and Regeneration, KU Leuven, Leuven, Belgium. silvia.monteagudo@kuleuven.be.ORCID 0000-0002-3849-6270

Funding

Fonds Wetenschappelijk Onderzoek (Research Foundation Flanders) 11L1822NFonds Wetenschappelijk Onderzoek (Research Foundation Flanders) 12AMS24NFonds Wetenschappelijk Onderzoek (Research Foundation Flanders) G056822NFonds Wetenschappelijk Onderzoek (Research Foundation Flanders) G059223NFonds Wetenschappelijk Onderzoek (Research Foundation Flanders) G097118N
6 · The paper itself

Abstract

Osteoarthritis is the most common joint disease and a global leading cause of pain and disability. Current treatment is limited to symptom relief, yet there is no disease-modifying therapy. Its multifactorial etiology includes excessive activation of Wnt signaling, but how Wnt causes joint destruction remains poorly understood. Here, we identify that Wnt signaling promotes the transcription of insulin-like growth factor 1 (IGF1) in articular chondrocytes and that IGF1 is a major driver of Wnt-induced joint damage. Male mice with cartilage-specific Igf1 deficiency are protected from Wnt-triggered joint disease. Mechanistically, Wnt-induced IGF1 transcription depends on β-catenin and binding of Wnt transcription factor TCF4 to the IGF1 gene promoter. In a clinically relevant mouse model of post-traumatic osteoarthritis, cartilage-specific deletion of Igf1 protects against the disease in male mice. IGF1 silencing in chondrocytes from patients with osteoarthritis restores a healthy molecular profile. Our findings reveal that reducing Wnt-induced IGF1 is a potential therapeutic strategy for osteoarthritis.

Indexed as

beta CateninCartilage, ArticularChondrocytesInsulin-Like Growth Factor IOsteoarthritisWnt Signaling PathwayAnimalsDisease Models, AnimalHumansMaleMiceMice, Inbred C57BLMice, KnockoutPromoter Regions, Geneticbeta CateninIGF1 protein, humaninsulin-like growth factor-1, mouseInsulin-Like Growth Factor I

Identifiers

PMID39448593
PMCPMC11502680

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Registered trials

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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.