ArticleThe Journal of clinical investigation2017
Osteocyte-specific WNT1 regulates osteoblast function during bone homeostasis.
Article in The Journal of clinical investigation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers, 1 of them a synthesis that pooled it.
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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
110 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.
- Consequences of Aging on Bone.Aging and disease · 2023Pooled it
- MultilevelCurrent research in structural biology · 2026Article
- Identification of candidate receptors mediating the osteoanabolic influence of Wnt1.JBMR plus · 2026Article
- Osteoarthritis and dementia: contrasting disorders driven by mutual pathways of autophagy, mTOR, GLP-1, AMPK, Wnt, and WISP1.Expert review of clinical pharmacology · 2026Review
- Osteocyte Cell-Cell Communication Within and Beyond Bone.Current osteoporosis reports · 2026Review
- The m6Am methyltransferase PCIF1 promotes osteogenic differentiation of mesenchymal stem cells through stabilization of Wnt-related transcripts.PLoS biology · 2026Article
- Mechanotransduction and musculoskeletal regeneration: Molecular mechanisms and interdisciplinary applications.Genes & diseases · 2026Review
- Current advances of bone homeostasis imbalance in the cause of hereditary metabolic bone diseases.EFORT open reviews · 2026Review
- A Scaffold-Based 3D Culture Model Including Selected Osteoprogenitors for Bone Regeneration With Controlled Morphology.Stem cells international · 2026Article
- A NewHuman mutation · 2026Article
- Molecular drivers of osteogenesis imperfecta: a cellular and extracellular collagen disease.Clinical science (London, England : 1979) · 2025Review
- Article
- Use of Teriparatide, Denosumab, and Romosozumab in a Postpartum Monogenic Osteoporosis With aJCEM case reports · 2025Article
- Wnt family members regulating osteogenesis and their origins.Journal of bone and mineral metabolism · 2025Review
- Article
- Spatial Multi-omics Reveals the Role of the Wnt Modulator, Dkk2, in Palatogenesis'.Journal of dental research · 2024Article
- Update on the Genetics of Osteogenesis Imperfecta.Calcified tissue international · 2024Review
- Metabolic reprogramming in skeletal cell differentiation.Bone research · 2024Review
- O-GlcNAcylation in the osteoblast lineage-boosting the complexity of Wnt-stimulated bone formation.EMBO reports · 2024Article
- Multi-omics analyses reveal aberrant differentiation trajectory with WNT1 loss-of-function in type XV osteogenesis imperfecta.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
50 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Mutations in WNT1 cause osteogenesis imperfecta (OI) and early-onset osteoporosis, identifying it as a key Wnt ligand in human bone homeostasis. However, how and where WNT1 acts in bone are unclear. To address this mechanism, we generated late-osteoblast-specific and osteocyte-specific WNT1 loss- and gain-of-function mouse models. Deletion of Wnt1 in osteocytes resulted in low bone mass with spontaneous fractures similar to that observed in OI patients. Conversely, Wnt1 overexpression from osteocytes stimulated bone formation by increasing osteoblast number and activity, which was due in part to activation of mTORC1 signaling. While antiresorptive therapy is the mainstay of OI treatment, it has limited efficacy in WNT1-related OI. In this study, anti-sclerostin antibody (Scl-Ab) treatment effectively improved bone mass and dramatically decreased fracture rate in swaying mice, a model of global Wnt1 loss. Collectively, our data suggest that WNT1-related OI and osteoporosis are caused in part by decreased mTORC1-dependent osteoblast function resulting from loss of WNT1 signaling in osteocytes. As such, this work identifies an anabolic function of osteocytes as a source of Wnt in bone development and homoeostasis, complementing their known function as targets of Wnt signaling in regulating osteoclastogenesis. Finally, this study suggests that Scl-Ab is an effective genotype-specific treatment option for WNT1-related OI and osteoporosis.
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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.