ArticleThe Journal of clinical investigation2016
NOTCH signaling in skeletal progenitors is critical for fracture repair.
Article in The Journal of clinical investigation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 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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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
71 citing papers in PubMed, 121 citations in OpenAlex.
- Tetrahedral framework nucleic acids: Nanokeys unlocking a new era of precision biomedicine.Journal of advanced research · 2026Review
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- Evaluation of the Osteogenic Potential of a NOTCH1 Agonist and Poloxamer 407 Hydrogel Regarding Osteoblasts.Biology · 2026Article
- Biomaterial-mediated Cell Atlas: an insight from single-cell and spatial transcriptomics.Bioactive materials · 2025Review
- Accelerated Bone Healing via Electrical Stimulation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Structurally and Functionally Adaptive Biomimetic Periosteum: Materials, Fabrication, and Construction Strategies.Exploration (Beijing, China) · 2025Review
- Photobiomodulation promotes osteogenic differentiation of mesenchymal stem cells and increases P-Akt levels in vitro.Scientific reports · 2025Article
- Notch signaling in osteoblast progenitor cells is required for BMP-induced bone formation.Bone · 2025Article
- Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation.Journal of translational medicine · 2025Article
- Addressing the challenges of infectious bone defects: a review of recent advances in bifunctional biomaterials.Journal of nanobiotechnology · 2025Review
- Landscape analysis of m6A modification reveals the dysfunction of bone metabolism in osteoporosis mice.Heliyon · 2025Article
- Article
- Activation of Wnt signaling in human fracture callus and nonunion tissues.Bone reports · 2024Article
- Nanofiber-induced hierarchically-porous magnesium phosphate bone cements accelerate bone regeneration by inhibiting Notch signaling.Bioactive materials · 2024Article
- Vascular restoration through local delivery of angiogenic factors stimulates bone regeneration in critical size defects.Bioactive materials · 2024Article
- Endothelial to mesenchymal Notch signaling regulates skeletal repair.JCI insight · 2024Article
- Beyond Traditional Medicine: EVs-Loaded Hydrogels as a Game Changer in Disease Therapeutics.Gels (Basel, Switzerland) · 2024Review
- Nicotinamide mononucleotide enhances fracture healing by promoting skeletal stem cell proliferation.Theranostics · 2024Article
- DNA methylation-mediated Rbpjk suppression protects against fracture nonunion caused by systemic inflammation.The Journal of clinical investigation · 2023Article
- Spatial heterogeneity of bone marrow endothelial cells unveils a distinct subtype in the epiphysis.Nature cell biology · 2023Article
11 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Fracture nonunions develop in 10%-20% of patients with fractures, resulting in prolonged disability. Current data suggest that bone union during fracture repair is achieved via proliferation and differentiation of skeletal progenitors within periosteal and soft tissues surrounding bone, while bone marrow stromal/stem cells (BMSCs) and other skeletal progenitors may also contribute. The NOTCH signaling pathway is a critical maintenance factor for BMSCs during skeletal development, although the precise role for NOTCH and the requisite nature of BMSCs following fracture is unknown. Here, we evaluated whether NOTCH and/or BMSCs are required for fracture repair by performing nonstabilized and stabilized fractures on NOTCH-deficient mice with targeted deletion of RBPjk in skeletal progenitors, maturing osteoblasts, and committed chondrocytes. We determined that removal of NOTCH signaling in BMSCs and subsequent depletion of this population result in fracture nonunion, as the fracture repair process was normal in animals harboring either osteoblast- or chondrocyte-specific deletion of RBPjk. Together, this work provides a genetic model of a fracture nonunion and demonstrates the requirement for NOTCH and BMSCs in fracture repair, irrespective of fracture stability and vascularity.
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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.