ArticleInflammation2023
Macrophage-Derived TGF-β and VEGF Promote the Progression of Trauma-Induced Heterotopic Ossification.
Article in Inflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 39 citations in OpenAlex.
- 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
- Macrophage metabolism directs regenerative versus fibrotic healing through BMP signaling in the mouse digit tip.bioRxiv : the preprint server for biology · 2026Article
- PRMT6 is required for initiating and amplifying macrophage-induced inflammation in heterotopic ossification by increasing CCL2 expression.Bone research · 2026Article
- Angiogenesis in ossification of the posterior longitudinal ligament: progress from mechanism to targeted intervention.Frontiers in cell and developmental biology · 2026Review
- Single-cell omics reveals arg-1 as a key regulator of age-dependent macrophage-mediated cartilage repair.PloS one · 2026Article
- The IL-33/ST2 Axis Promotes Traumatic Heterotopic Ossification by Driving Macrophage and Mast Cell-Mediated Inflammation via Autophagy Defects.International journal of biological sciences · 2026Article
- Targeting macrophage-mediated TGF-β/BMP signaling in ankylosing spondylitis: from inflammation to pathological bone formation.Frontiers in immunology · 2026Review
- Biofunctionalization of Stem Cell Scaffold for Osteogenesis and Bone Regeneration.Biomolecules · 2025Review
- TGF-β signaling in heterotopic ossification: the pathogenesis and the target for its treatment.Journal of orthopaedic surgery and research · 2025Review
- Single cell RNA-seq analysis associates Osm signaling in macrophages with osteogenic differentiation during heterotopic ossification.Journal of orthopaedic surgery and research · 2025Article
- POSTN-Mediated Interplay of M1 Polarized Macrophage with Tendon-Derived Stem Cells to Drive Traumatic Heterotopic Ossification Formation through PTK7/ATK Signaling?Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- GPR40 activation alleviates pulmonary fibrosis by repressing M2 macrophage polarization through the PKD1/CD36/TGF-β1 pathway.Acta pharmacologica Sinica · 2025Article
- When Bone Forms Where It Shouldn't: Heterotopic Ossification in Muscle Injury and Disease.International journal of molecular sciences · 2025Review
- Macrophage Polarization in Heterotopic Ossification: Inflammation, Osteogenesis, and Emerging Therapeutic Targets.International journal of molecular sciences · 2025Review
- Article
- Preclinical validation of TGFβ inhibitors as a novel therapeutic strategy for post-traumatic heterotopic ossification.Scientific reports · 2025Article
- A375 melanoma-derived lactate controls A375 melanoma phenotypes by inducing macrophage M2 polarizationPeerJ · 2025Article
- Review
- The Role of Neuromodulation and Potential Mechanism in Regulating Heterotopic Ossification.Neurochemical research · 2024Review
- Intersections of Fibrodysplasia Ossificans Progressiva and Traumatic Heterotopic Ossification.Biomolecules · 2024Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heterotopic ossification (HO) is a pathological bone formation process caused by musculoskeletal trauma. HO is characterized by aberrant endochondral ossification and angiogenesis. Our previous studies have indicated that macrophage inflammation is involved in traumatic HO formation. In this study, we found that macrophage infiltration and TGF-β signaling activation are presented in human HO. Depletion of macrophages effectively suppressed traumatic HO formation in a HO mice model, and macrophage depletion significantly inhibited the activation of TGF-β/Smad2/3 signaling. In addition, the TGF-β blockade created by a neutralizing antibody impeded ectopic bone formation in vivo. Notably, endochondral ossification and angiogenesis are attenuated following macrophage depletion or TGF-β inhibition. Furthermore, our observations on macrophage polarization revealed that M2 macrophages, rather than M1 macrophages, play a critical role in supporting HO development by enhancing the osteogenic and chondrogenic differentiation of mesenchymal stem cells. Our findings on ectopic bone formation in HO patients and the mice model indicate that M2 macrophages are an important contributor for HO development, and that inhibition of M2 polarization or TGF-β activity may be a potential method of therapy for traumatic 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.