ArticleThe Journal of clinical investigation2020
Immobilization after injury alters extracellular matrix and stem cell fate.
Article in The Journal of clinical investigation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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
48 citing papers in PubMed, 74 citations in OpenAlex.
- Dietary omega-6 lipids promote postinjury aberrant bone formation in obesity.The Journal of clinical investigation · 2026Article
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- Beyond Potency: Emerging Determinants and Optimization Strategies Enhancing Therapeutic Efficacy of Adult Stem Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- Early detection of aberrant cell fate and repair using circulating progenitor cells in patients with heterotopic ossification.Nature communications · 2026Article
- Thrombospondin 1 and 2 regulate mesenchymal progenitor cell fate and matrix organization.Bone research · 2026Article
- Integrin-mediated SPP1 signaling from macrophages orchestrates extracellular matrix remodeling and chondrogenesis in heterotopic ossification.Journal of translational medicine · 2025Article
- Nicheformer: a foundation model for single-cell and spatial omics.Nature methods · 2025Article
- When Bone Forms Where It Shouldn't: Heterotopic Ossification in Muscle Injury and Disease.International journal of molecular sciences · 2025Review
- Macrophage response to fibrin structure mediated by Tgm2-dependent mitochondrial mechanosensing.Bioactive materials · 2025Article
- 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
- Heterotopic ossification: Current developments and emerging potential therapies.Chinese medical journal · 2025Review
- Polycystin-1 regulates tendon-derived mesenchymal stem cells fate and matrix organization in heterotopic ossification.Bone research · 2025Article
- A CD26Nature communications · 2025Article
- Article
- Multi-omics Analysis to Identify Key Immune Genes for Osteoporosis based on Machine Learning and Single-cell Analysis.Orthopaedic surgery · 2024Article
- Diatomite-incorporated hierarchical scaffolds for osteochondral regeneration.Bioactive materials · 2024Article
- The roles of Hippo/YAP signaling pathway in physical therapy.Cell death discovery · 2024Review
- The HIF-1α/PLOD2 axis integrates extracellular matrix organization and cell metabolism leading to aberrant musculoskeletal repair.Bone research · 2024Article
- Article
- Enhanced BMP signaling in Cathepsin K-positive tendon progenitors induces heterotopic ossification.Biochemical and biophysical research communications · 2023Article
Corrections and comments
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Authors and funding
21 authors at 5 institutions in 4 countries.
Funding
Abstract
Cells sense the extracellular environment and mechanical stimuli and translate these signals into intracellular responses through mechanotransduction, which alters cell maintenance, proliferation, and differentiation. Here we use a mouse model of trauma-induced heterotopic ossification (HO) to examine how cell-extrinsic forces impact mesenchymal progenitor cell (MPC) fate. After injury, single-cell (sc) RNA sequencing of the injury site reveals an early increase in MPC genes associated with pathways of cell adhesion and ECM-receptor interactions, and MPC trajectories to cartilage and bone. Immunostaining uncovers active mechanotransduction after injury with increased focal adhesion kinase signaling and nuclear translocation of transcriptional coactivator TAZ, inhibition of which mitigates HO. Similarly, joint immobilization decreases mechanotransductive signaling, and completely inhibits HO. Joint immobilization decreases collagen alignment and increases adipogenesis. Further, scRNA sequencing of the HO site after injury with or without immobilization identifies gene signatures in mobile MPCs correlating with osteogenesis, and signatures from immobile MPCs with adipogenesis. scATAC-seq in these same MPCs confirm that in mobile MPCs, chromatin regions around osteogenic genes are open, whereas in immobile MPCs, regions around adipogenic genes are open. Together these data suggest that joint immobilization after injury results in decreased ECM alignment, altered MPC mechanotransduction, and changes in genomic architecture favoring adipogenesis over osteogenesis, resulting in decreased formation of 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.