ArticleFrontiers in immunology2019
Inhibition of JAK1/2 Tyrosine Kinases Reduces Neurogenic Heterotopic Ossification After Spinal Cord Injury.
Article in Frontiers in immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 44 citations in OpenAlex.
- Comprehensive analysis of mRNA-microRNA-lncRNA expression profiles in post-traumatic elbow heterotopic ossification using RNA sequencing and experimental validation.Annals of medicine · 2026Article
- M1 macrophage-derived CXCL12 drives neurogenic heterotopic ossification following spinal cord injury.Neural regeneration research · 2026Article
- Neurogenic heterotopic ossification: from molecular mechanisms to clinical treatment.Journal of orthopaedic translation · 2026Review
- STAT3 Signaling in Spinal Cord Injury: Neurochemical Mechanisms Linking Neuroinflammation, Mitochondrial Stress, and Glial Remodeling.Neurochemical research · 2026Review
- Heterotopic Ossification: Molecular Drivers, Subtype-Specific Mechanisms, and Translational Therapeutic Advances.Biomolecules · 2026Review
- Many but not all pathogen-associated molecular patterns aggravate neurogenic heterotopic ossification after spinal cord injury.Journal of biomedical science · 2026Article
- Intermittent and Short-Term Empirical Ruxolitinib Regimen for Steroid-Refractory Flareups of Fibrodysplasia Ossificans Progressiva.Pharmacology research & perspectives · 2025Article
- Macrophage Polarization in Heterotopic Ossification: Inflammation, Osteogenesis, and Emerging Therapeutic Targets.International journal of molecular sciences · 2025Review
- Single-cell sequencing systematically analyzed the mechanism of Emdogain on the restoration of delayed replantation periodontal membrane.International journal of oral science · 2025Article
- Heterotopic ossification: Current developments and emerging potential therapies.Chinese medical journal · 2025Review
- Bu Yang Huan Wu Prevents Osteogenic Effect of Muscle-Derived Stromal Cells via Regulating JAK/STAT Pathway.Journal of cellular and molecular medicine · 2025Article
- A glucocorticoid spike derails muscle repair to heterotopic ossification after spinal cord injury.Cell reports. Medicine · 2024Article
- Spatiotemporal Analysis of Mesenchymal Stem Cells Fate Determination by Inflammatory Niche Following Soft Tissue Injury at a Single-Cell Level.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Oncostatin M promotes osteogenic differentiation of tendon-derived stem cells through the JAK2/STAT3 signalling pathway.Journal of orthopaedic surgery and research · 2024Article
- Cell Senescence in Heterotopic Ossification.Biomolecules · 2024Review
- Immunologic Aspects in Fibrodysplasia Ossificans Progressiva.Biomolecules · 2024Review
- M1 macrophage-derived oncostatin M induces osteogenic differentiation of ligamentum flavum cells through the JAK2/STAT3 pathway.JOR spine · 2024Article
- Interorgan communication in neurogenic heterotopic ossification: the role of brain-derived extracellular vesicles.Bone research · 2024Article
- Oncostatin M: Dual Regulator of the Skeletal and Hematopoietic Systems.Current osteoporosis reports · 2024Review
- Spinal cord injury dysregulates fibro-adipogenic progenitors miRNAs signaling to promote neurogenic heterotopic ossifications.Communications biology · 2023Article
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neurogenic heterotopic ossifications (NHO) are very incapacitating complications of traumatic brain and spinal cord injuries (SCI) which manifest as abnormal formation of bone tissue in periarticular muscles. NHO are debilitating as they cause pain, partial or total joint ankylosis and vascular and nerve compression. NHO pathogenesis is unknown and the only effective treatment remains surgical resection, however once resected, NHO can re-occur. To further understand NHO pathogenesis, we developed the first animal model of NHO following SCI in genetically unmodified mice, which mimics most clinical features of NHO in patients. We have previously shown that the combination of (1) a central nervous system lesion (SCI) and (2) muscular damage (via an intramuscular injection of cardiotoxin) is required for NHO development. Furthermore, macrophages within the injured muscle play a critical role in driving NHO pathogenesis. More recently we demonstrated that macrophage-derived oncostatin M (OSM) is a key mediator of both human and mouse NHO. We now report that inflammatory monocytes infiltrate the injured muscles of SCI mice developing NHO at significantly higher levels compared to mice without SCI. Muscle infiltrating monocytes and neutrophils expressed OSM whereas mouse muscle satellite and interstitial cell expressed the OSM receptor (OSMR).
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