ArticleBone research2024
Interorgan communication in neurogenic heterotopic ossification: the role of brain-derived extracellular vesicles.
Article in Bone research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 14 citations in OpenAlex.
- Tibial bone compression promotes recovery after brain injury through osteocyte PIEZO1.Nature neuroscience · 2026Article
- Adrenomedullin from spinal cord injury drives heterotopic ossification in skeletal muscle via a neuro-immune-bone axis.Experimental & molecular medicine · 2026Article
- Neurogenic heterotopic ossification: from molecular mechanisms to clinical treatment.Journal of orthopaedic translation · 2026Review
- Brain-bone Crosstalk after Neurotrauma: Dual Effects of Traumatic Brain Injury on Skeletal Remodeling.Current osteoporosis reports · 2026Review
- Heterotopic Ossification: Molecular Drivers, Subtype-Specific Mechanisms, and Translational Therapeutic Advances.Biomolecules · 2026Review
- PKM2 from hyperactive neuron aggravate lung injury post-stroke by promoting FOXO3A/TXNIP mitochondria translocation in mice.Redox biology · 2026Article
- Machine Learning-Based Text Processing Reveals Research Trends in Heterotopic Ossification.Analytical cellular pathology (Amsterdam) · 2026Article
- Plasma-derived exosomes from obese knee osteoarthritis aggravate synovitis by promoting cellular senescence of synovial fibroblasts.Journal of orthopaedic translation · 2026Article
- Extracellular vesicles originating from induced pluripotent stem cell-derived chondrocytes facilitate the regeneration of osteoarthritic cartilage.Journal of orthopaedic translation · 2026Article
- Review
- Pak4-mediated crosstalk between necroptotic macrophages and tendon stem/progenitor cells contributes to traumatic heterotopic ossification formation.Bone research · 2025Article
- Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Risk factors for the development of heterotopic ossification of the elbow in children with untreated chronic Monteggia fractures: a radiographic review of 274 cases.Journal of orthopaedics and traumatology : official journal of the Italian Society of Orthopaedics and Traumatology · 2025Article
- Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Engineered melatonin-pretreated plasma exosomes repair traumatic spinal cord injury by regulating miR-138-5p/SOX4 axis mediated microglia polarization.Journal of orthopaedic translation · 2024Article
- Extracellular Vesicles: A Crucial Player in the Intestinal Microenvironment and Beyond.International journal of molecular sciences · 2024Review
- Recent progress of methods for cuproptosis detection.Frontiers in molecular biosciences · 2024Review
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain-derived extracellular vesicles participate in interorgan communication after traumatic brain injury by transporting pathogens to initiate secondary injury. Inflammasome-related proteins encapsulated in brain-derived extracellular vesicles can cross the blood‒brain barrier to reach distal tissues. These proteins initiate inflammatory dysfunction, such as neurogenic heterotopic ossification. This recurrent condition is highly debilitating to patients because of its relatively unknown pathogenesis and the lack of effective prophylactic intervention strategies. Accordingly, a rat model of neurogenic heterotopic ossification induced by combined traumatic brain injury and achillotenotomy was developed to address these two issues. Histological examination of the injured tendon revealed the coexistence of ectopic calcification and fibroblast pyroptosis. The relationships among brain-derived extracellular vesicles, fibroblast pyroptosis and ectopic calcification were further investigated in vitro and in vivo. Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk reversed the development of neurogenic heterotopic ossification in vivo. The present work highlights the role of brain-derived extracellular vesicles in the pathogenesis of neurogenic heterotopic ossification and offers a potential strategy for preventing neurogenic heterotopic ossification after traumatic brain injury. Brain-derived extracellular vesicles (BEVs) are released after traumatic brain injury. These BEVs contain pathogens and participate in interorgan communication to initiate secondary injury in distal tissues. After achillotenotomy, the phagocytosis of BEVs by fibroblasts induces pyroptosis, which is a highly inflammatory form of lytic programmed cell death, in the injured tendon. Fibroblast pyroptosis leads to an increase in calcium and phosphorus concentrations and creates a microenvironment that promotes osteogenesis. Intravenous injection of the pyroptosis inhibitor Ac-YVAD-cmk suppressed fibroblast pyroptosis and effectively prevented the onset of heterotopic ossification after neuronal injury. The use of a pyroptosis inhibitor represents a potential strategy for the treatment of neurogenic heterotopic ossification.
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