ArticleBone reports2022
The role of hypertrophic chondrocytes in regulation of the cartilage-to-bone transition in fracture healing.
Article in Bone reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed, 39 citations in OpenAlex.
- Fracture healing: from molecular and cellular mechanisms to therapeutic strategies.Signal transduction and targeted therapy · 2026Review
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- Metallic topological structures in bone repair implants: Design, properties, and biological interactions.Journal of orthopaedic translation · 2026Review
- A spatiotemporal atlas of senescence-associated secretory phenotype in fracture healing: stage-dependent mechanisms and therapeutic windows.Inflammation and regeneration · 2026Review
- Modeling the chondrocyte-derived osteoblasts formation process reveals its molecular signature and regulation network.Bone research · 2026Article
- Tooth-bone attachment tissue is produced by cells with a mixture of odontoblastic and osteoblastic features in reptiles.Journal of anatomy · 2026Article
- APEX1, a transcriptional hub for endochondral ossification and fracture repair.Bone research · 2026Article
- Biologics for bone regeneration: advances in cell, protein, gene, and mRNA therapies.Bone research · 2026Review
- Cytosolic phospholipase A2 as a therapeutic target for degenerative joint diseases.Bone research · 2025Article
- An ingenious design from nature to accelerate the repair of long-bone critical defects: the longitudinal tubular transverse interconnection structure of deer antlers.Materials today. Bio · 2025Article
- Mechanism of Piezo1 regulating chondrocyte mitochondrial function and promoting fracture healing through β-catenin/LARS2 signaling pathway.Bone research · 2025Article
- The Effects and Mechanisms of Low-Intensity Pulsed Ultrasound on Bone Remodeling: From Laboratory to Clinic.Biomolecules · 2025Review
- Osteoarthritis as an evolutionary legacy: Biological ageing and chondrocyte hypertrophy.Osteoarthritis and cartilage open · 2025Review
- Effects of Peripheral Magnetic Stimulation on Bone Healing After Fractures in Mice.Calcified tissue international · 2025Article
- Article
- Co-Culture Approaches in Cartilage and Bone Tissue Regeneration.International journal of molecular sciences · 2025Review
- Callus organoids reveal distinct cartilage to bone transition mechanisms across donors and a role for biological sex.Bone research · 2025Article
- TP8, A Novel Chondroinductive Peptide, Significantly Promoted Neo-Cartilage Repair without Activating Bone Formation.Advanced healthcare materials · 2025Article
- Communication between endothelial cells and osteoblasts in regulation of bone homeostasis: Notch players.Stem cell research & therapy · 2025Review
- Deer antler velvet (Cervus elaphus sibiricus) promotes fracture healing via partial BMP2-Smad mediated osteoblast differentiation.Journal of orthopaedic surgery and research · 2025Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Endochondral bone formation is an important pathway in fracture healing, involving the formation of a cartilaginous soft callus and the process of cartilage-to-bone transition. Failure or delay in the cartilage-to-bone transition causes an impaired bony union such as nonunion or delayed union. During the healing process, multiple types of cells including chondrocytes, osteoprogenitors, osteoblasts, and endothelial cells coexist in the callus, and inevitably crosstalk with each other. Hypertrophic chondrocytes located between soft cartilaginous callus and bony hard callus mediate the crosstalk regulating cell-matrix degradation, vascularization, osteoclast recruitment, and osteoblast differentiation in autocrine and paracrine manners. Furthermore, hypertrophic chondrocytes can become osteoprogenitors and osteoblasts, and directly contribute to woven bone formation. In this review, we focus on the roles of hypertrophic chondrocytes in fracture healing and dissect the intermingled crosstalk in fracture callus during the cartilage-to-bone transition.
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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.