ArticleDevelopment (Cambridge, England)2016
FGF signaling in the osteoprogenitor lineage non-autonomously regulates postnatal chondrocyte proliferation and skeletal growth.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
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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.
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.
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Who cites it
44 citing papers in PubMed, 74 citations in OpenAlex.
- Recapitulating Endochondral Ossification for Bone Repair: From Development to Engineering Strategy.Advanced healthcare materials · 2026Review
- Divergent Mechanisms of Cranial Suture Ossification in Normal Development and Pathologic Fusion.Journal of cellular and molecular medicine · 2026Review
- The heterozygous c.2241G>C variation in FGFR2 may cause autosomal dominant Kirner's deformity in a Chinese Han pedigree.BMC medical genomics · 2026Article
- Spatiotemporal Regulation and Lineage Specification in Embryonic Endochondral Ossification.International journal of molecular sciences · 2026Review
- Review
- Resolving the design principles that control post-natal vascular growth and scaling.Cell systems · 2025Article
- Further Evidence of Early-Onset Osteoporosis and Bone Fractures as a NewInternational journal of molecular sciences · 2025Article
- Drug-Loaded Bioscaffolds for Osteochondral Regeneration.Pharmaceutics · 2024Review
- Review of published 467 achondroplasia patients: clinical and mutational spectrum.Orphanet journal of rare diseases · 2024Review
- An FGFR2 mutation as the potential cause of a new phenotype including early-onset osteoporosis and bone fractures: a case report.BMC medical genomics · 2023Article
- 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
- Novel Insights Into the Genetic Causes of Short Stature in Children.TouchREVIEWS in endocrinology · 2022Review
- Growth and mechanobiology of the tendon-bone enthesis.Seminars in cell & developmental biology · 2022Review
- 4PBA reduces growth deficiency in osteogenesis imperfecta by enhancing transition of hypertrophic chondrocytes to osteoblasts.JCI insight · 2022Article
- Deletion of Fibroblast growth factor 9 globally and in skeletal muscle results in enlarged tuberosities at sites of deltoid tendon attachments.Developmental dynamics : an official publication of the American Association of Anatomists · 2021Article
- Tissue Engineering Strategies to Increase Osteochondral Regeneration of Stem Cells; a Close Look at Different Modalities.Stem cell reviews and reports · 2021Review
- Importance of WNT-dependent signaling for derivation and maintenance of primed pluripotent bovine embryonic stem cells†.Biology of reproduction · 2021Article
- Advantages and Disadvantages of Different Treatment Methods in Achondroplasia: A Review.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Fibroblast growth factor (FGF) signaling is important for skeletal development; however, cell-specific functions, redundancy and feedback mechanisms regulating bone growth are poorly understood. FGF receptors 1 and 2 (Fgfr1 and Fgfr2) are both expressed in the osteoprogenitor lineage. Double conditional knockout mice, in which both receptors were inactivated using an osteoprogenitor-specific Cre driver, appeared normal at birth; however, these mice showed severe postnatal growth defects that include an ∼50% reduction in body weight and bone mass, and impaired longitudinal bone growth. Histological analysis showed reduced cortical and trabecular bone, suggesting cell-autonomous functions of FGF signaling during postnatal bone formation. Surprisingly, the double conditional knockout mice also showed growth plate defects and an arrest in chondrocyte proliferation. We provide genetic evidence of a non-cell-autonomous feedback pathway regulating Fgf9, Fgf18 and Pthlh expression, which led to increased expression and signaling of Fgfr3 in growth plate chondrocytes and suppression of chondrocyte proliferation. These observations show that FGF signaling in the osteoprogenitor lineage is obligately coupled to chondrocyte proliferation and the regulation of longitudinal bone growth.
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Registered trials
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.