ArticleBone research2025
RUNX2 is essential for maintaining synchondrosis chondrocytes and cranial base growth.
Article in Bone research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Cranial Base Morphology and Mandibular Growth in Skeletal Deep Bite: A Longitudinal Study in Prepubertal Children.Diagnostics (Basel, Switzerland) · 2026Article
- Exploring the role ofFrontiers in physiology · 2026Article
- Review
- The Multifaceted Role of miR-211 in Health and Disease.Biomolecules · 2025Review
- Effects of selenium-mediated RUNX2 overexpression and its transcriptome alterations on Chondrocyte injury in Kashin Beck disease.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
The cranial base synchondroses, comprised of opposite-facing bidirectional chondrocyte layers, drive anteroposterior cranial base growth. In humans, RUNX2 haploinsufficiency causes cleidocranial dysplasia associated with deficient midfacial growth. However, how RUNX2 regulates chondrocytes in the cranial base synchondroses remains unknown. To address this, we inactivated Runx2 in postnatal synchondrosis chondrocytes using a tamoxifen-inducible Fgfr3-creER (Fgfr3-Runx2
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Registered trials
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