ArticleBone2018
Gli1-labeled adult mesenchymal stem/progenitor cells and hedgehog signaling contribute to endochondral heterotopic ossification.
Article in Bone, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
- Heterotopic Ossification: Molecular Drivers, Subtype-Specific Mechanisms, and Translational Therapeutic Advances.Biomolecules · 2026Review
- Ectodysplasin-A (EDA) Signaling Cross-Talk in Skeletogenesis.Calcified tissue international · 2026Review
- Early detection of aberrant cell fate and repair using circulating progenitor cells in patients with heterotopic ossification.Nature communications · 2026Article
- GNAS/PKA signaling promotes aberrant osteochondral differentiation of Gli1The EMBO journal · 2025Article
- Regulation of Skeletogenic Pathways by m6A RNA Modification: A Comprehensive Review.Calcified tissue international · 2025Review
- 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
- Discoidin domain receptor 2 is an important modulator of BMP signaling during heterotopic bone formation.Bone research · 2025Article
- 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
- Heterotopic Ossifications Following Intramedullary Stabilization of Femoral Fractures in Polytraumatized Patients.Journal of clinical medicine · 2024Review
- Gli1 labels progenitors during chondrogenesis in postnatal mice.EMBO reports · 2024Article
- Phase separation of SHP2E76K promotes malignant transformation of mesenchymal stem cells by activating mitochondrial complexes.JCI insight · 2024Article
- Inhibition of PI3K/AKT signaling pathway prevents blood-induced heterotopic ossification of the injured tendon.Journal of orthopaedic translation · 2024Article
- Role of hedgehog signaling in the pathogenesis and therapy of heterotopic ossification.Frontiers in cell and developmental biology · 2024Review
- Metformin alleviates genetic and traumatic heterotopic ossification by inhibiting infiltration and mitochondrial metabolism of myeloid cells.American journal of translational research · 2024Article
- Tppp3Bone research · 2023Article
- Activated fibroblasts in cancer: Perspectives and challenges.Cancer cell · 2023Review
- Post-traumatic heterotopic ossification in front of the ankle joint for 23 years: A case report and review of literature.World journal of clinical cases · 2023Article
- Fetuin-A is an immunomodulator and a potential therapeutic option in BMP4-dependent heterotopic ossification and associated bone mass loss.Bone research · 2022Article
- Acetabular Reaming Is a Reliable Model to Produce and Characterize Periarticular Heterotopic Ossification of the Hip.Stem cells translational medicine · 2022Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Heterotopic ossification (HO), acquired or hereditary, endochondral or intramembranous, is the formation of true bone outside the normal skeleton. Since perivascular Gli1+ progenitors contribute to injury induced organ fibrosis, and CD133 is expressed by a variety of populations of adult stem cells, this study utilized Cre-lox based genetic lineage tracing to test the contribution to endochondral HO of adult stem/progenitor cells that expressed either Gli1 or CD133. We found that both lineages contributed broadly to different normal tissues with distinct patterns, but that only Gli1-creERT labeled stem/progenitor cells contributed to all stages of endochondral HO in a BMP dependent, injury induced, transgenic mouse model. Hedgehog (Hh) signaling was abnormal at endochondral HO lesion sites with increased signaling surrounding the lesion but diminished signaling within it. Thus, local dysregulation of Hh signaling participates in the pathophysiology of endochondral HO. However, unlike a previous report of intramembranous HO, systemic inhibition of Hh signaling was insufficient to prevent the initiation of the endochondral HO process or to treat the existing endochondral HO, suggesting that Hh participates in, but is not essential for endochondral HO in this model. This could potentially reflect the underlying difference between intramembranous and endochondral HO. Nevertheless, identification of this novel stem/precursor cell population as a HO-contributing cell population provides a potential drugable target.
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