ArticlePloS one2015
Activation of HIFa pathway in mature osteoblasts disrupts the integrity of the osteocyte/canalicular network.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Recent Advances in the Role of Osteocytes in Orthodontic Tooth Movement.International journal of molecular sciences · 2025Review
- Hypoxia-activated oxidative stress mediates SHP2/PI3K signaling pathway to promote hepatocellular carcinoma growth and metastasis.Scientific reports · 2025Article
- Preclinical Rodent Models for Human Bone Disease, Including a Focus on Cortical Bone.Endocrine reviews · 2024Review
- Article
- FRZB affectsExperimental and therapeutic medicine · 2023Article
- Contributions of Resin Cast Etching to Visualising the Osteocyte Lacuno-Canalicular Network Architecture in Bone Biology and Tissue Engineering.Calcified tissue international · 2023Review
- Hypoxia Pathway in Osteoporosis: Laboratory Data for Clinical Prospects.International journal of environmental research and public health · 2023Review
- Review
- Deletion ofFrontiers in immunology · 2022Article
- Osteocytic HIF-1α Pathway Manipulates Bone Micro-structure and Remodeling via Regulating Osteocyte Terminal Differentiation.Frontiers in cell and developmental biology · 2021Article
- The Effects of Sclerostin on the Immune System.Current osteoporosis reports · 2020Review
- Wnt Antagonists in Hematopoietic and Immune Cell Fate: Implications for Osteoporosis Therapies.Current osteoporosis reports · 2019Review
- Article
- Article
- Hormonal Regulation of Osteocyte Perilacunar and Canalicular Remodeling in the Hyp Mouse Model of X-Linked Hypophosphatemia.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The hypoxia-inducible factors (HIFs), HIF-1α and HIF-2α, are the central mediators of the homeostatic response that enables cells to survive and differentiate in low-oxygen conditions. Previous studies indicated that disruption of the von Hippel-Lindau gene (Vhl) coincides with the activation of HIFα signaling. Here we show that inactivation of Vhl in mature osteoblasts/osteocytes induces their apoptosis and disrupts the cell/canalicular network. VHL-deficient (ΔVHL) mice exhibited a significantly increased cortical bone area resulting from enhanced proliferation and osteogenic differentiation of the bone marrow stromal cells (BMSCs) by inducing the expression of β-catenin in the BMSC. Our data suggest that the VHL/HIFα pathway in mature osteoblasts/osteocytes plays a critical role in the bone cell/canalicular network and that the changes of osteocyte morphology/function and cell/canalicular network may unleash the bone formation, The underlying mechanism of which was the accumulation of β-catenin in the osteoblasts/osteoprogenitors of the bone marrow.
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