ArticleFrontiers in endocrinology2022
Aberrant activation of TGF-β1 induces high bone turnover
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A case-based explainable graph neural network framework for mechanistic drug repositioning.Bioinformatics (Oxford, England) · 2026Article
- Genetics and pathophysiology of diffuse idiopathic skeletal hyperostosis.Frontiers in endocrinology · 2026Review
- Revealing the Diagnostic Potential of Three RHO GTPase-Related Genes in Osteoarthritis Based on Single-Cell RNA Sequencing and GEO Dataset Analysis.International journal of genomics · 2026Article
- Direct and indirect effects of transforming growth factor-beta on osteoclast-mediated bone remodeling using a new in vitro bone matrix model.JBMR plus · 2025Article
- Serum IL-6 and TGF-β1 concentrations as diagnostic biomarkers in elderly male patients with osteoporosis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2025Article
- TNF receptor-associated factors: promising targets of natural products for the treatment of osteoporosis.Frontiers in physiology · 2025Review
- Article
- TGF-β1 Inhibits Osteoclast Differentiation and Abnormal Angiogenesis in Intervertebral Disc Degeneration: Evidence from RNA Sequencing and Animal Studies.Orthopaedic surgery · 2024Article
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Authors and funding
13 authors.
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Abstract
In the adult skeleton, the bone remodeling process involves a dynamic coordination between osteoblasts and osteoclasts, which is disrupted in diseases with high bone turnover rates and dysregulated transforming growth factor beta 1 (TGF-β1). However, little is known about how TGF-β1 signaling mediates bone resorption. Here, we described a pedigree with a heterozygous variant in TGF-β1 (R218C) that resulted in aberrant activation of TGF-β1 through an activating mechanism that caused Camurati-Engelmann disease (CED). We showed that CED patients have high levels of active Rho GTPases and the migration-related proteins Integrin β1 and Integrin β3 in their peripheral blood. HEK293T cells transfected with a plasmid encoding this mutant expressed high levels of TGF-β1 and active Rho GTPases. Furthermore, activation of Rho by TGF-β1 increased osteoclast formation and bone resorption, with increased migration of pre-osteoclasts, as well as cytoskeletal remodeling of pre-osteoclasts and mature osteoclasts. Importantly, pharmacological inhibition of Rho GTPases effectively rescued hyperactive TGF-β1-induced osteoclastogenesis
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