ArticleThe Journal of clinical investigation2018
Aberrant TGF-β activation in bone tendon insertion induces enthesopathy-like disease.
Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- A Systematic Review of Animal Models of Disuse-Induced Bone Loss.Calcified tissue international · 2021Pooled it
- Macrophage Derived TGF-β Recruits BMSCs for Initiation of Bone Formation During Fracture Healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Mechanical gating of tendon fibrogenic transcription in systemic sclerosis.Nature communications · 2026Article
- TGF-β/BMP signaling in skeletal biology: molecular mechanisms, regulatory networks, and therapeutic implications in development, regeneration, and disease.Bone research · 2026Review
- Temporal vascular pattern remodeling mediated by the FHL2/sFRP2 signaling pathway in tenocytes affects tendon repair and regeneration.Experimental & molecular medicine · 2025Article
- Proton-activated chloride channel increases endplate porosity and pain in a mouse spine degeneration model.The Journal of clinical investigation · 2024Article
- A role for TGFβ signaling in Gli1+ tendon and enthesis cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024Review
- Murine Hind Limb Explant Model for Studying the Mechanobiology of Achilles Tendon Impingement.Journal of visualized experiments : JoVE · 2023Article
- Silk protein sericin: a promising therapy for Achilles tendinopathy-evidence from an experimental rat model.Clinical rheumatology · 2023Article
- The bone marrow side of axial spondyloarthritis.Nature reviews. Rheumatology · 2023Review
- Neutralization of excessive levels of active TGF-β1 reduces MSC recruitment and differentiation to mitigate peritendinous adhesion.Bone research · 2023Article
- Review of Basic Research about Ossification of the Spinal Ligaments Focusing on Animal Models.Journal of clinical medicine · 2023Review
- Hot spots and frontiers in bone-tendon interface research: a bibliometric analysis and visualization from 2000 to 2023.Frontiers in surgery · 2023Review
- Engineered Decellularized Tendon Matrix Putty Preserves Native Tendon Bioactivity to Promote Cell Proliferation and Enthesis Repair.Journal of tissue engineering and regenerative medicine · 2023Article
- Partial Tendon Injury at the Tendon-to-Bone Enthesis Activates Skeletal Stem Cells.Stem cells translational medicine · 2022Article
- CXCL12/CXCR4-Rac1-mediated migration of osteogenic precursor cells contributes to pathological new bone formation in ankylosing spondylitis.Science advances · 2022Article
- Inhibition of Integrin αvβ6 Activation of TGF-β Attenuates Tendinopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- The effects of intra-ovarian autologous platelet rich plasma injection on IVF outcomes of poor responder women and women with premature ovarian insufficiencyJournal of the Turkish German Gynecological Association · 2022Article
- Biomimetic strategies for tendon/ligament-to-bone interface regeneration.Bioactive materials · 2021Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Enthesopathy is a disorder of bone, tendon, or ligament insertion. It represents one-fourth of all tendon-ligament diseases and is one of the most difficult tendon-ligament disorders to treat. Despite its high prevalence, the exact pathogenesis of this condition remains unknown. Here, we show that TGF-β was activated in both a semi-Achilles tendon transection (SMTS) mouse model and in a dorsiflexion immobilization (DI) mouse model of enthesopathy. High concentrations of active TGF-β recruited mesenchymal stromal stem cells (MSCs) and led to excessive vessel formation, bone deterioration, and fibrocartilage calcification. Transgenic expression of active TGF-β1 in bone also induced enthesopathy with a phenotype similar to that observed in SMTS and DI mice. Systemic inhibition of TGF-β activity by injection of 1D11, a TGF-β-neutralizing antibody, but not a vehicle antibody, attenuated the excessive vessel formation and restored uncoupled bone remodeling in SMTS mice. 1D11-treated SMTS fibrocartilage had increased proteoglycan and decreased collagen X and matrix metalloproteinase 13 expression relative to control antibody treatment. Notably, inducible knockout of the TGF-β type II receptor in mouse MSCs preserved the bone microarchitecture and fibrocartilage composition after SMTS relative to the WT littermate controls. Thus, elevated levels of active TGF-β in the enthesis bone marrow induce the initial pathological changes of enthesopathy, indicating that TGF-β inhibition could be a potential therapeutic strategy.
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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.