ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2014
Runx2 regulates endochondral ossification through control of chondrocyte proliferation and differentiation.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 163 citations in OpenAlex.
- RUNX2 inhibitor CADD522 improves bone microarchitecture and lipid metabolism in post-menopausal bone loss.npj drug discovery · 2026Article
- Recapitulating Endochondral Ossification for Bone Repair: From Development to Engineering Strategy.Advanced healthcare materials · 2026Review
- Mechanobiology of hypertrophic chondrocyte mineralization: Biomechanical regulation and therapeutic implications in skeletal disorders.Mechanobiology in medicine · 2026Review
- Exploring Growth Pattern and Candidate Genes for Chicken Spur.Animals : an open access journal from MDPI · 2026Article
- A Vascularized Microphysiological System Reproducing Endochondral Ossification in Vitro to Study Ewing Sarcoma Proliferation and Migration.Advanced functional materials · 2026Article
- Midpalatal suture expansion: an in vivo histological and immunohistochemical study of the impact of force magnitude.Acta odontologica latinoamericana : AOL · 2025Article
- Multilayer dual-porosity 3D printed scaffolds to recreate the anisotropic microenvironment of the hyaline cartilage.Materials today. Bio · 2025Article
- RUNX2 is essential for maintaining synchondrosis chondrocytes and cranial base growth.Bone research · 2025Article
- TRIB3 mediates vascular calcification by facilitating self-ubiquitination and dissociation of Smurf1 in chronic kidney disease.The Journal of clinical investigation · 2025Article
- In Vitro Engineered ECM-incorporated Hydrogels for Osteochondral Tissue Repair: A Cell-Free Approach.Advanced healthcare materials · 2025Article
- miRNA-based regulation in growth plate cartilage: mechanisms, targets, and therapeutic potential.Frontiers in endocrinology · 2025Review
- Development of novel osteoarthritis therapy by targeting AMPK-β-catenin-Runx2 signaling.Genes & diseases · 2025Review
- The Biphasic Activity of Auricularia Auricula-Judae Extract on Bone Homeostasis through Inhibition of Osteoclastogenesis and Modulation of Osteogenic Activity.Journal of microbiology and biotechnology · 2024Article
- Pathogenesis and Management Strategies in Radioiodine-Refractory Differentiated Thyroid Cancer: From Molecular Mechanisms Toward Therapeutic Approaches: A Comprehensive Review.Journal of clinical medicine · 2024Review
- Regulation of Skeletal Development and Maintenance by Runx2 and Sp7.International journal of molecular sciences · 2024Review
- The role of semaphorin 3A on chondrogenic differentiation.In vitro cellular & developmental biology. Animal · 2024Article
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- A synthetic, closed-looped gene circuit for the autonomous regulation of RUNX2 activity during chondrogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
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- Commitment of human mesenchymal stromal cells to skeletal lineages is independent of their morphogenetic capacity.World journal of stem cells · 2023Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Synthesis of cartilage by chondrocytes is an obligatory step for endochondral ossification. Global deletion of the Runx2 gene results in complete failure of the ossification process, but the underlying cellular and molecular mechanisms are not fully known. Here, we elucidated Runx2 regulatory control distinctive to chondrocyte and cartilage tissue by generating Runx2 exon 8 floxed mice. Deletion of Runx2 gene in chondrocytes caused failure of endochondral ossification and lethality at birth. The limbs of Runx2(ΔE8/ΔE8) mice were devoid of mature chondrocytes, vasculature, and marrow. We demonstrate that the C-terminus of Runx2 drives its biological activity. Importantly, nuclear import and DNA binding functions of Runx2 are insufficient for chondrogenesis. Molecular studies revealed that despite normal levels of Sox9 and PTHrP, chondrocyte differentiation and cartilage growth are disrupted in Runx2(ΔE8/ΔE8) mice. Loss of Runx2 in chondrocytes also impaired osteoprotegerin-receptor activator of NF-κB ligand (OPG-RANKL) signaling and chondroclast development. Dwarfism observed in Runx2 mutants was associated with the near absence of proliferative zone in the growth plates. Finally, we show Runx2 directly regulates a unique set of cell cycle genes, Gpr132, Sfn, c-Myb, and Cyclin A1, to control proliferative capacity of chondrocyte. Thus, Runx2 is obligatory for both proliferation and differentiation of chondrocytes.
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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.