ArticleEMBO molecular medicine2020
Aberrant upregulation of CaSR promotes pathological new bone formation in ankylosing spondylitis.
Article in EMBO molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Adrenomedullin from spinal cord injury drives heterotopic ossification in skeletal muscle via a neuro-immune-bone axis.Experimental & molecular medicine · 2026Article
- JAK Inhibitor Tofacitinib Ameliorates Inflammation Response and Osteogenic Differentiation in Immune-Mediated Inflammatory Arthritis in Rats.International journal of rheumatic diseases · 2026Article
- Research Advances on the Mechanism and Diagnosis of Bone Bridging in Ankylosing Spondylitis.Orthopedic research and reviews · 2026Review
- Upregulated GDF-15 in Ankylosing Spondylitis: Pathologic Ossification Promotion through Ligament Fibroblast Osteogenic Differentiation.ACR open rheumatology · 2025Article
- The function of GPCRs in different bone cells.International journal of biological sciences · 2025Review
- Research progress on cellular behavior of CaSR in cardiovascular diseases.Frontiers in immunology · 2025Review
- Research Review on the Mechanisms of Pathological New Bone Formation in Ankylosing Spondylitis.Orthopedic research and reviews · 2025Review
- Patients with ankylosing spondylitis present a distinct CD8 T cell subset with osteogenic and cytotoxic potential.RMD open · 2024Article
- CD_99 G1 neutrophils modulate osteogenic differentiation of mesenchymal stem cells in the pathological process of ankylosing spondylitis.Annals of the rheumatic diseases · 2024Article
- MYC: there is more to it than cancer.Frontiers in cell and developmental biology · 2024Review
- Treating thoracic-lumbar Andersson lesion in patients with ankylosing spondylitis: case series.Annals of medicine and surgery (2012) · 2023Article
- MYC promotes fibroblast osteogenesis by regulating ALP and BMP2 to participate in ectopic ossification of ankylosing spondylitis.Arthritis research & therapy · 2023Article
- CXCL12/CXCR4-Rac1-mediated migration of osteogenic precursor cells contributes to pathological new bone formation in ankylosing spondylitis.Science advances · 2022Article
- The calcium-sensing receptor in inflammation: Recent updates.Frontiers in physiology · 2022Review
- Punicalagin Regulates Signaling Pathways in Inflammation-Associated Chronic Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Juvenile Spondyloarthritis: What More Do We Know About HLA-B27, Enthesitis, and New Bone Formation?Frontiers in medicine · 2021Review
- Immunopathophysiology of Juvenile Spondyloarthritis (jSpA): The "Out of the Box" View on Epigenetics, Neuroendocrine Pathways and Role of the Macrophage Migration Inhibitory Factor (MIF).Frontiers in medicine · 2021Review
- CaSR-Mediated hBMSCs Activity Modulation: Additional Coupling Mechanism in Bone Remodeling Compartment.International journal of molecular sciences · 2020Article
- Aberrant upregulation of CaSR promotes pathological new bone formation in ankylosing spondylitis.EMBO molecular medicine · 2020Article
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Authors and funding
15 authors at 1 institution in 1 country.
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Abstract
Pathological new bone formation is a typical pathological feature in ankylosing spondylitis (AS), and the underlying molecular mechanism remains elusive. Previous studies have shown that the calcium-sensing receptor (CaSR) is critical for osteogenic differentiation while also being highly involved in many inflammatory diseases. However, whether it plays a role in pathological new bone formation of AS has not been reported. Here, we report the first piece of evidence that expression of CaSR is aberrantly upregulated in entheseal tissues collected from AS patients and animal models with different hypothetical types of pathogenesis. Systemic inhibition of CaSR reduced the incidence of pathological new bone formation and the severity of the ankylosing phenotype in animal models. Activation of PLCγ signalling by CaSR promoted bone formation both in vitro and in vivo. In addition, various inflammatory cytokines induced upregulation of CaSR through NF-κB/p65 and JAK/Stat3 pathways in osteoblasts. These novel findings suggest that inflammation-induced aberrant upregulation of CaSR and activation of CaSR-PLCγ signalling in osteoblasts act as mediators of inflammation, affecting pathological new bone formation in AS.
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