ArticleDevelopment (Cambridge, England)2017
Cartilage to bone transformation during fracture healing is coordinated by the invading vasculature and induction of the core pluripotency genes.
Article in Development (Cambridge, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 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.
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Who cites it
147 citing papers in PubMed, 212 citations in OpenAlex.
- The regulatory significance of chondrocyte hypertrophy in maintaining chondrocyte homeostasis, regeneration and repair.Future science OA · 2026Review
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Loss of MCT1 mediated lactate uptake causes delayed endplate maturation and intervertebral disc degeneration.Cell death & disease · 2026Article
- Construction of pre-vascularized bone-like tissue by incorporation of mesodermal progenitor cells through simulating endochondral ossification.Stem cell research & therapy · 2026Article
- A Modular Bioinstructive Platform Reveals Mechanistic Insights into Additive-Free, Topography-Driven Osteogenesis.Advanced healthcare materials · 2026Article
- Could alteration in the vacuum phenomenon rather than its presence be a sign of spinal instability?European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Article
- Advanced multifunctional thermo- and electro-stimulative hydrogels for bone regeneration.Materials today. Bio · 2026Review
- Murine Progeria Model Exhibits Delayed Fracture Healing With Senescent Phenotype and Dysregulated Immune Response.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Stage-resolved geography of mouse skeletal stem cells.Journal of bone and mineral metabolism · 2026Review
- Modeling the chondrocyte-derived osteoblasts formation process reveals its molecular signature and regulation network.Bone research · 2026Article
- Multi-omics-informed hydrogel design: modulating IL-6 to reduce endoplasmic reticulum stress in bone regeneration.Bioactive materials · 2026Article
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- Piezo1 in hypertrophic chondrocytes regulates osteoclastogenesis in endochondral ossification.International journal of biological sciences · 2026Article
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- Mesenchymal progenitor-derived proteoglycan 4 regulates the transdifferentiation of chondrocytes into osteoblasts during fracture healing.Stem cells translational medicine · 2025Article
- Effects of Peripheral Magnetic Stimulation on Bone Healing After Fractures in Mice.Calcified tissue international · 2025Article
- Endothelial-mesenchymal crosstalk drives osteogenic differentiation of human osteoblasts through Notch signaling.Cell communication and signaling : CCS · 2025Article
- Communication between endothelial cells and osteoblasts in regulation of bone homeostasis: Notch players.Stem cell research & therapy · 2025Review
- FGFR antagonists restore defective mandibular bone repair in a mouse model of osteochondrodysplasia.Bone research · 2025Article
- Deep behavioral phenotyping tracks functional recovery following tibia fracture in mice.Frontiers in physiology · 2025Article
87 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Fractures heal predominantly through the process of endochondral ossification. The classic model of endochondral ossification holds that chondrocytes mature to hypertrophy, undergo apoptosis and new bone forms by invading osteoprogenitors. However, recent data demonstrate that chondrocytes transdifferentiate to osteoblasts in the growth plate and during regeneration, yet the mechanism(s) regulating this process remain unknown. Here, we show a spatially-dependent phenotypic overlap between hypertrophic chondrocytes and osteoblasts at the chondro-osseous border in the fracture callus, in a region we define as the transition zone (TZ). Hypertrophic chondrocytes in the TZ activate expression of the pluripotency factors [Sox2, Oct4 (Pou5f1), Nanog], and conditional knock-out of Sox2 during fracture healing results in reduction of the fracture callus and a delay in conversion of cartilage to bone. The signal(s) triggering expression of the pluripotency genes are unknown, but we demonstrate that endothelial cell conditioned medium upregulates these genes in ex vivo fracture cultures, supporting histological evidence that transdifferentiation occurs adjacent to the vasculature. Elucidating the cellular and molecular mechanisms underlying fracture repair is important for understanding why some fractures fail to heal and for developing novel therapeutic interventions.
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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.