ArticleBone2019
Persistent Sox9 expression in hypertrophic chondrocytes suppresses transdifferentiation into osteoblasts.
Article in Bone, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
41 citing papers in PubMed, 52 citations in OpenAlex.
- TNAP and PHOSPHO1 Function Synergistically to Afford Critical Control Over the Mineralization of the Postnatal Murine Skeleton.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Chondrocytes in fracture healing: A review of chondrocyte journey.Chinese medical journal · 2026Review
- miR-433 targets BMP and Indian hedgehog signaling to coordinate murine postnatal growth plate dynamics.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026Article
- Inhibition of FGFR signaling with infigratinib improves linear bone growth in the femaleJBMR plus · 2026Article
- TNAP and PHOSPHO1 function synergistically to afford critical control over the mineralisation of the postnatal murine skeleton.bioRxiv : the preprint server for biology · 2026Article
- SMN deficiency inhibits endochondral ossification via promoting TRAF6-induced ubiquitination degradation of YBX1 in spinal muscular atrophy.Bone research · 2025Article
- Stem cell-based cartilage regeneration: Biological strategies, engineering innovations, and clinical translation.World journal of stem cells · 2025Review
- Mesenchymal Stem Cell-Derived Extracellular Vesicles: Seeking into Cell-Free Therapies for Bone-Affected Lysosomal Storage Disorders.International journal of molecular sciences · 2025Review
- RUNX2 is essential for maintaining synchondrosis chondrocytes and cranial base growth.Bone research · 2025Article
- Deciphering cartilage neuro-immune interactions and innervation profile through 3D engineered osteoarthritic micropathophysiological system.Materials today. Bio · 2025Article
- SOX9 haploinsufficiency reveals SOX9-Noggin interaction in BMP-SMAD signaling pathway in chondrogenesis.Cellular and molecular life sciences : CMLS · 2025Article
- The IFITM5 mutation in osteogenesis imperfecta type V is associated with an ERK/SOX9-dependent osteoprogenitor differentiation defect.The Journal of clinical investigation · 2024Article
- Hnrnpk protects against osteoarthritis through targeting WWC1 mRNA and inhibiting Hippo signaling pathway.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Thy-1 knockdown promotes the osteogenic differentiation of GMSCs via the Wnt/β-catenin pathway.Journal of cellular and molecular medicine · 2023Article
- Altered Sox9 and FGF signaling gene expression in Aga2 OI mice negatively affects linear growth.JCI insight · 2023Article
- The emerging studies on mesenchymal progenitors in the long bone.Cell & bioscience · 2023Review
- Genome-wide association study reveals that the IBSP locus affects ear size in cattle.Heredity · 2023Article
- Article
- Article
- Direct Reprogramming of Mouse Subchondral Bone Osteoblasts into Chondrocyte-like Cells.Biomedicines · 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 1 institution in 1 country.
Funding
Abstract
Longitudinal bone growth is driven by endochondral ossification, a process in which cartilage tissue is generated by growth plate chondrocytes and then remodeled into bone by osteoblasts. In the postnatal growth plate, as hypertrophic chondrocytes approach the chondro-osseous junction, they may undergo apoptosis, or directly transdifferentiate into osteoblasts. The molecular mechanisms governing this switch in cell lineage are poorly understood. Here we show that the physiological downregulation of Sox9 in hypertrophic chondrocyte is associated with upregulation of osteoblast-associated genes (such as Mmp13, Cola1, Ibsp) in hypertrophic chondrocytes, before they enter the metaphyseal bone. In transgenic mice that continued to express Sox9 in all cells derived from the chondrocytic lineage, upregulation of these osteoblast-associated genes in the hypertrophic zone failed to occur. Furthermore, lineage tracing experiments showed that, in transgenic mice expressing Sox9, the number of chondrocytes transdifferentiating into osteoblasts was markedly reduced. Collectively, our findings suggest that Sox9 downregulation in hypertrophic chondrocytes promotes expression of osteoblast-associated genes in hypertrophic chondrocytes and promotes the subsequent transdifferentiation of these cells into osteoblasts.
Indexed as
Identifiers
What OpenQuestion holds
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.