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Study · Animal study (in vivo) · mouse · 2025

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FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.

Morice A, de La Seiglière A, Kany A, Khonsari RH, Bensidhoum M, Puig-Lombardi ME, Legeai Mallet L

Bone research21 Jan 2025Cited by 5 (Europe PMC)

PMID39837840 (opens in a new tab)PMCIDPMC11751307 (opens in a new tab)DOI10.1038/s41413-024-00385-x (opens in a new tab)PepBankPUB-39837840
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Summary

Gain-of-function mutations in fibroblast growth factor receptor (FGFR) genes lead to chondrodysplasia and craniosynostoses. FGFR signaling has a key role in the formation and repair of the craniofacial skeleton. Here, we analyzed the impact of Fgfr2- and Fgfr3-activating mutations on mandibular bone formation and endochondral bone repair after non-stabilized mandibular fractures in mouse models of Crouzon syndrome (Crz) and hypochondroplasia (Hch). Bone mineralization of the calluses was abnormally high in Crz mice and abnormally low in Hch mice. The latter model presented pseudarthrosis and impaired chondrocyte differentiation. Spatial transcriptomic analyses of the Hch callus revealed abnormally low expression of Col11, Col1a, Dmp1 genes in mature chondrocytes. We found that the expression of genes involved in autophagy and apoptosis (Smad1, Comp, Birc2) was significantly perturbed and that the Dusp3, Dusp9, and Socs3 genes controlling the mitogen-activated protein kinase pathway were overexpressed. Lastly, we found that treatment with a tyrosine kinase inhibitor (BGJ398, infigratinib) or a C-type natriuretic peptide (BMN111, vosoritide) fully rescued the defective endochondral bone repair observed in Hch mice. Taken as a whole, our findings show that FGFR3 is a critical orchestrator of bone repair and provide a rationale for the development of potential treatments for patients with FGFR3-osteochondrodysplasia.
CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study1

1 result from studies that gave the peptide. No result from this study comes from people.

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In hypochondroplasia mice, vosoritide fully rescued defective endochondral bone repair.

    In plain wordsIn mice with hypochondroplasia, vosoritide fully restored defective bone repair.

    Peptide
    Vosoritide
    Outcome
    IncreaseEndochondral bone repair
    Study

    mousen: not reported in source

    Hypochondroplasia mouse model with mandibular fractures
    Outcome group
    Bone and joint · Musculoskeletal
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Lastly, we found that treatment with a tyrosine kinase inhibitor (BGJ398, infigratinib) or a C-type natriuretic peptide (BMN111, vosoritide) fully rescued the defective endochondral bone repair observed in Hch mice.
    1 context sentence
    Summary · context
    Here, we analyzed the impact of Fgfr2- and Fgfr3-activating mutations on mandibular bone formation and endochondral bone repair after non-stabilized mandibular fractures in mouse models of Crouzon syndrome (Crz) and hypochondroplasia (Hch).

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Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

  1. Version 2Current

    28 Oct 2026, 02:03 UTC

    Study results updated

  2. Version 1

    27 Oct 2026, 16:37 UTC

    First added · source update from Europe PMC

Subjects

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