ArticleNature communications2018
Inhibition of overactive TGF-β attenuates progression of heterotopic ossification in mice.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 152 papers.
What it found
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The trial behind it
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Who cites it
152 citing papers in PubMed, 225 citations in OpenAlex.
- M1 macrophage-derived CXCL12 drives neurogenic heterotopic ossification following spinal cord injury.Neural regeneration research · 2026Article
- Stiff-yet-tough glassy hydrogels for tendon rupture repair.Bioactive materials · 2026Article
- Pathogenic transcriptional reprogramming of fibro-adipogenic progenitors in mice with FOP and its mitigation by inhibition of ACVR1 and activin A.bioRxiv : the preprint server for biology · 2026Article
- Piezo2FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Integrative Transcriptomic Profiling Delineates LTBP4-Driven Fibroblast Reprogramming Across the Ossification Continuum of the Ligamentum Flavum.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- A NON-CANONICAL ROLE FOR NOTCH3 IN BUILDING THE INTESTINAL LYMPHATIC NICHE.bioRxiv : the preprint server for biology · 2026Article
- A modular self-assembling peptide platform targeting TGF-β1 for tendon regeneration.Nature communications · 2026Article
- 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
- Ceramide-PKCζ signaling axis mediates burn-enhanced ectopic calcification during Achilles tendon healing.Journal of molecular histology · 2026Article
- Identification of a Tenochondral Ossification Sequence Producing Heterotopic Ossification in Human Achilles Tendinopathy.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2026Article
- Heterotopic Ossification: Molecular Drivers, Subtype-Specific Mechanisms, and Translational Therapeutic Advances.Biomolecules · 2026Review
- Ubiquitin-specific protease 26 facilitates endochondral ossification by driving chondrocyte hypertrophy and mineralization.Bone research · 2026Article
- Primary Cilia Are Required for Efficient BMP Signaling in Traumatic Heterotopic Ossification.Biomedicines · 2026Article
- PRMT6 is required for initiating and amplifying macrophage-induced inflammation in heterotopic ossification by increasing CCL2 expression.Bone research · 2026Article
- Activin A secretion by muscle-repairing macrophages induces heterotopic ossification in mice.The Journal of clinical investigation · 2026Article
- TGF-β-induced fibrotic scar formation limits recovery of spinal cord injury.Bone research · 2026Article
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- PJ34 Prevents Trauma-Induced Heterotopic Ossification without Adverse Bone Healing: An in vivo and in vitro Investigation.Drug design, development and therapy · 2026Article
- Angiogenesis in ossification of the posterior longitudinal ligament: progress from mechanism to targeted intervention.Frontiers in cell and developmental biology · 2026Review
- Genetics and pathophysiology of diffuse idiopathic skeletal hyperostosis.Frontiers in endocrinology · 2026Review
92 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 2 countries.
Funding
Abstract
Acquired heterotopic ossification (HO) is a painful and debilitating disease characterized by extraskeletal bone formation after injury. The exact pathogenesis of HO remains unknown. Here we show that TGF-β initiates and promotes HO in mice. We find that calcified cartilage and newly formed bone resorb osteoclasts after onset of HO, which leads to high levels of active TGF-β that recruit mesenchymal stromal/progenitor cells (MSPCs) in the HO microenvironment. Transgenic expression of active TGF-β in tendon induces spontaneous HO, whereas systemic injection of a TGF-β neutralizing antibody attenuates ectopic bone formation in traumatic and BMP-induced mouse HO models, and in a fibrodysplasia ossificans progressive mouse model. Moreover, inducible knockout of the TGF-β type II receptor in MSPCs inhibits HO progression in HO mouse models. Our study points toward elevated levels of active TGF-β as inducers and promoters of ectopic bone formation, and suggest that TGF-β might be a therapeutic target in HO.
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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.