ArticleDevelopment (Cambridge, England)2016
β-catenin activity in late hypertrophic chondrocytes locally orchestrates osteoblastogenesis and osteoclastogenesis.
Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 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
52 citing papers in PubMed, 77 citations in OpenAlex.
- Oxygen‑sensing histone demethylase KDM6A modulates chondrocyte‑to‑osteoblast transdifferentiation by activating the Wnt/β‑catenin pathway.International journal of molecular medicine · 2026Article
- Nf2 orchestrates β-arrestin2-biased PTH1R signaling to couple bone mass with skeletal integrity.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cell signaling and transcriptional regulation of osteoclast lineage commitment, differentiation, bone resorption and diseases.Cell discovery · 2026Review
- Gender inequality in osteoarthritis: a bioinformatics perspective.Clinical rheumatology · 2026Article
- Piezo1 in hypertrophic chondrocytes regulates osteoclastogenesis in endochondral ossification.International journal of biological sciences · 2026Article
- Descendants of hypertrophic chondrocytes promote angiogenesis by secreting THBS4 during bone growth and injury repair.Bone research · 2025Article
- Article
- PTPN11 in cartilage development, adult homeostasis, and diseases.Bone research · 2025Review
- Single-cell RNA-seq reveals a repair pattern in cystic lesions in steroid induced osteonecrosis of the femoral head.Frontiers in immunology · 2025Article
- Compensatory growth and recovery of cartilage cytoarchitecture after transient cell death in fetal mouse limbs.Nature communications · 2024Article
- Article
- The Origin and Fate of Chondrocytes: Cell Plasticity in Physiological Setting.Current osteoporosis reports · 2023Review
- Article
- AXIN1 bi-allelic variants disrupting the C-terminal DIX domain cause craniometadiaphyseal osteosclerosis with hip dysplasia.American journal of human genetics · 2023Article
- The emerging studies on mesenchymal progenitors in the long bone.Cell & bioscience · 2023Review
- Article
- A Shifting Paradigm: Transformation of Cartilage to Bone during Bone Repair.Journal of dental research · 2023Review
- The role of hypertrophic chondrocytes in regulation of the cartilage-to-bone transition in fracture healing.Bone reports · 2022Article
- Close-to-native bone repair via tissue-engineered endochondral ossification approaches.iScience · 2022Review
- Hnrnpk maintains chondrocytes survival and function during growth plate development via regulating Hif1α-glycolysis axis.Cell death & disease · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trabecular bone formation is the last step in endochondral ossification. This remodeling process of cartilage into bone involves blood vessel invasion and removal of hypertrophic chondrocytes (HTCs) by chondroclasts and osteoclasts. Periosteal- and chondrocyte-derived osteoprogenitors utilize the leftover mineralized HTC matrix as a scaffold for primary spongiosa formation. Here, we show genetically that β-catenin (encoded by Ctnnb1), a key component of the canonical Wnt pathway, orchestrates this remodeling process at multiple levels. Conditional inactivation or stabilization of β-catenin in HTCs by a Col10a1-Cre line locally modulated osteoclastogenesis by altering the Rankl:Opg ratio in HTCs. Lack of β-catenin resulted in a severe decrease of trabecular bone in the embryonic long bones. Gain of β-catenin activity interfered with removal of late HTCs and bone marrow formation, leading to a continuous mineralized hypertrophic core in the embryo and resulting in an osteopetrotic-like phenotype in adult mice. Furthermore, β-catenin activity in late HTCs is required for chondrocyte-derived osteoblastogenesis at the chondro-osseous junction. The latter contributes to the severe trabecular bone phenotype in mutants lacking β-catenin activity in HTCs.
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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.