ArticleBiology open2026
Dkk1 inhibition restores mandibular growth in an achondroplasia mouse model.
Article in Biology open, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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.
Who cites it
1 citing paper in PubMed.
- From FGFR3 Hyperactivation to Disease-Modifying Therapy in Pediatric Achondroplasia: Molecular Mechanisms, Clinical Evidence, and Emerging Treatments.Children (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
Meckel's and condylar cartilages are key to mandible development, with Meckel's cartilage acting as a template and condylar cartilage as a growth center. In achondroplasia, the most common form of genetic dwarfism, abnormalities of these cartilages lead to micrognathia, with significant functional repercussions for affected individuals. How FGFR3 overactivation in achondroplasia disrupts Meckel's and condylar cartilages is largely unknown. Our aim was to identify the pathways driving these disruptions by analyzing the genes expressed in these cartilages in a mouse model mimicking achondroplasia. Using cartilage laser-microdissection and RNA-sequencing analyses, we first compared the transcriptome of Meckel's and condylar cartilages from E16.5 embryos of control and Fgfr3Y367C/+ mice. Over 900 genes were differentially expressed, including the Dkk1 gene, which encodes an inhibitor of β-catenin-dependent Wnt signaling and was significantly overexpressed in chondrocytes of Fgfr3 mutants in both Meckel's and condylar cartilages. Immunostaining of sections of the cartilages confirmed the high expression at the protein level. Primary cultures of Meckel's cartilage chondrocytes showed that, in Fgfr3Y367C/+ mutants, activation of the canonical Wnt pathway with Wnt3a was reduced, while a Dkk1 antagonist increased Wnt activity, suggesting that Dkk1 overexpression was responsible for decreased canonical Wnt activity in mutants. In a mandible organ culture model, inhibition of Dkk1 also significantly increased the mandible size, due to an increased elongation of the condylar cartilage of mutants, as seen after tissue clearing and Sox9 immunolabeling. In this cartilage, increased proliferation and defective differentiation into hypertrophic chondrocytes was partially corrected by Dkk1 inhibition. Our data suggest that dysregulation of Wnt/β-catenin activity due to Fgfr3 gain-of function mutation constitutes an important underlying mechanism in craniofacial defects observed in achondroplasia.
Indexed as
Identifiers
What OpenQuestion holds
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.