ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2021
Deletion of Fibroblast growth factor 9 globally and in skeletal muscle results in enlarged tuberosities at sites of deltoid tendon attachments.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Genetic Susceptibility to Sport-Related Muscle Injuries: Insights from the Literature and Novel Gene Candidates.International journal of molecular sciences · 2025Review
- Loss of Fgfr1 and Fgfr2 in Scleraxis-lineage cells leads to enlarged bone eminences and attachment cell death.Developmental dynamics : an official publication of the American Association of Anatomists · 2023Article
- Targeted deletion of Fgf9 in tendon disrupts mineralization of the developing enthesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- New developments in the biology of fibroblast growth factors.WIREs mechanisms of disease · 2022Review
- Cervical vertebrae fusion in elbow knee synostosis (Eks)-mutant mice with fibroblast growth factor 9 N143T mutation.Congenital anomaliesArticle
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe growth of most bony tuberosities, like the deltoid tuberosity (DT), rely on the transmission of muscle forces at the tendon-bone attachment during skeletal growth. Tuberosities distribute muscle forces and provide mechanical leverage at attachment sites for joint stability and mobility. The genetic factors that regulate tuberosity growth remain largely unknown. In mouse embryos with global deletion of fibroblast growth factor 9 (Fgf9), the DT size is notably enlarged. In this study, we explored the tissue-specific regulation of DT size using both global and targeted deletion of Fgf9.
resultsWe showed that cell hypertrophy and mineralization dynamics of the DT, as well as transcriptional signatures from skeletal muscle but not bone, were influenced by the global loss of Fgf9. Loss of Fgf9 during embryonic growth led to increased chondrocyte hypertrophy and reduced cell proliferation at the DT attachment site. This endured hypertrophy and limited proliferation may explain the abnormal mineralization patterns and locally dysregulated expression of markers of endochondral development in Fgf9
conclusionTaken together, we discovered that Fgf9 may play an influential role in muscle-bone cross-talk during embryonic and postnatal development.
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