ArticlePloS one2013
Load regulates bone formation and Sclerostin expression through a TGFβ-dependent mechanism.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- Prognostic and therapeutic potential of microRNAs for fracture healing processes and non-union fractures: A systematic review.Clinical and translational medicine · 2023Pooled it
- A soft diet attenuates exercise-induced increases in cortical bone density and formation in long bones in growing mice.Scientific reports · 2026Article
- Spatially resolved osteoblast-traced transcriptomics uncovers TGF-β as a combination target with sclerostin in osteoporosis.Bone research · 2026Article
- Research Progress on Dance Training as a Mechanical Stimulus for the Prevention and Treatment of Osteoporosis: A Narrative Review.International journal of molecular sciences · 2026Review
- Association Between Sclerostin and Sarcopenia-Related Functional Decline in Older Women.Diagnostics (Basel, Switzerland) · 2026Article
- Sending the Signal to Bone: How Tumor-Derived EVs Orchestrate Pre-Metastatic Niche Formation and Skeletal Colonization.Biomedicines · 2025Review
- The role of osteopontin and osteocyte-derived factors in secondary hyperparathyroidism-induced myopathy.JBMR plus · 2024Article
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β-dependent control of osteocyte function.JCI insight · 2024Article
- Ubiquitin-specific peptidases: Players in bone metabolism.Cell proliferation · 2023Review
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Fat, adipokines, bone structure and bone regulatory factors associations in obesity.European journal of endocrinology · 2022Observational
- Resident Self-Tissue of Proinflammatory Cytokines Rather Than Their Systemic Levels Correlates with Development of Myelofibrosis inBiomolecules · 2022Article
- Review
- Sclerostin and Its Involvement in the Pathogenesis of Idiopathic Scoliosis.Journal of clinical medicine · 2021Review
- Mechanosensitive miR-100 coordinates TGFβ and Wnt signaling in osteocytes during fluid shear stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Treadmill exercise influences the microRNA profiles in the bone tissues of mice.Experimental and therapeutic medicine · 2021Article
- Disrupted osteocyte connectivity and pericellular fluid flow in bone with aging and defective TGF-β signaling.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Osteocyte Dysfunction in Joint Homeostasis and Osteoarthritis.International journal of molecular sciences · 2021Review
- Osteocytes as main responders to low-intensity pulsed ultrasound treatment during fracture healing.Scientific reports · 2021Article
- Mechanosensitive Control of Articular Cartilage and Subchondral Bone Homeostasis in Mice Requires Osteocytic Transforming Growth Factor β Signaling.Arthritis & rheumatology (Hoboken, N.J.) · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Bone continually adapts to meet changing physical and biological demands. Osteoblasts, osteoclasts, and osteocytes cooperate to integrate these physical and biochemical cues to maintain bone homeostasis. Although TGFβ acts on all three of these cell types to maintain bone homeostasis, the extent to which it participates in the adaptation of bone to mechanical load is unknown. Here, we investigated the role of the TGFβ pathway in load-induced bone formation and the regulation of Sclerostin, a mechanosensitive antagonist of bone anabolism. We found that mechanical load rapidly represses the net activity of the TGFβ pathway in osteocytes, resulting in reduced phosphorylation and activity of key downstream effectors, Smad2 and Smad3. Loss of TGFβ sensitivity compromises the anabolic response of bone to mechanical load, demonstrating that the mechanosensitive regulation of TGFβ signaling is essential for load-induced bone formation. Furthermore, sensitivity to TGFβ is required for the mechanosensitive regulation of Sclerostin, which is induced by TGFβ in a Smad3-dependent manner. Together, our results show that physical cues maintain bone homeostasis through the TGFβ pathway to regulate Sclerostin expression and the deposition of new bone.
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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.