ArticleMolecular therapy. Nucleic acids2019
miR-17-5p Regulates Heterotopic Ossification by Targeting ANKH in Ankylosing Spondylitis.
Article in Molecular therapy. Nucleic acids, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Review
- Overexpression of Circ_0004496 is Associated with Pathological Bone Formation in Ankylosing Spondylitis via the miR-145/ACTG1 Axis.Balkan medical journal · 2026Article
- Aloe vera gel extract and bone marrow mesenchymal stem cells ameliorate thioacetamide-induced liver fibrosis via modulating lincRNA-p21/miR-17-5p axis.Anatomy & cell biology · 2026Article
- miR-17-5p: bridging the gap between disease mechanisms and therapeutic innovations.Epigenomics · 2025Review
- Overexpression of miR17 ~ 92 in Myeloid Cells in Mice Increased Bone Mass Through Reduced Bone Resorption and Increased Bone Formation in Sex-Dependent Manner.Calcified tissue international · 2025Article
- Fibroblasts in heterotopic ossification: mechanisms and therapeutic targets.International journal of biological sciences · 2025Review
- Article
- Targeting fibroblasts in pathological bone formation: mechanisms and treatments.Frontiers in cell and developmental biology · 2025Review
- The role of miRNAs as biomarkers in heterotopic ossification.EFORT open reviews · 2024Review
- Jianpi Qingre Tongluo Decoction exerted an anti-inflammatory effect on AS by inhibiting the NONHSAT227927.1/JAK2/STAT3 axis.Heliyon · 2024Article
- Environmental and Genetic Determinants of Ankylosing Spondylitis.International journal of molecular sciences · 2024Review
- Sequence of Events in the Pathogenesis of Axial Spondyloarthritis: A Current Review-2023 SPARTAN Meeting Proceedings.Current rheumatology reports · 2024Review
- Triptolide alleviates the development of inflammation in ankylosing spondylitis via the NONHSAT227927.1/JAK2/STAT3 pathway.Experimental and therapeutic medicine · 2024Article
- Spinal cord injury dysregulates fibro-adipogenic progenitors miRNAs signaling to promote neurogenic heterotopic ossifications.Communications biology · 2023Article
- MiRNAs as Potential Regulators of Enthesis Healing: Findings in a Rodent Injury Model.International journal of molecular sciences · 2023Article
- Fibroblast Insights into the Pathogenesis of Ankylosing Spondylitis.Journal of inflammation research · 2023Review
- The role of miRNA and lncRNA in heterotopic ossification pathogenesis.Stem cell research & therapy · 2022Review
- Circ_0018168 inhibits the proliferation and osteogenic differentiation of fibroblasts in ankylosing spondylitis via regulating miR-330-3p/DKK1 axis.Regenerative therapy · 2022Article
- Modulation of Small RNA Signatures by Astrocytes on Early Neurodegeneration Stages; Implications for Biomarker Discovery.Life (Basel, Switzerland) · 2022Review
- Pathophysiology and Emerging Molecular Therapeutic Targets in Heterotopic Ossification.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ankylosing spondylitis (AS) is a chronic inflammatory disease characterized with heterotopic ossification of the axis joints ligaments, resulting in joint disability. MicroRNAs (miRNAs) are regulators of mRNAs that play a crucial role in the AS pathological process. Here, we showed that the level of miR-17-5p was significantly higher in fibroblasts and ligament tissues from AS patients as compared to the non-AS individuals. Knockdown of the miR-17-5p from the fibroblasts derived from AS patients exhibited decreased osteogenic differentiation and ossification. On the other hand, AS patient-derived fibroblasts overexpressing miR-17-5p displayed the increased osteogenesis. Furthermore, inhibition of miR-17-5p ameliorated osteophyte formation, and the sacroiliitis phenotype in AS rats received emulsified collagen. Mechanistically, miR-17-5p regulated osteogenic differentiation by targeting the 3' UTR of ankylosis protein homolog (ANKH). Also, downregulation of miR-17-5p slowed AS progression through regulation of cytokines, such as dickkopf-1 (DKK1) and vascular endothelial growth factor (VEGF). In conclusion, our findings reveal a role of the miR-17-5p-ANKH axis in the regulation of heterotopic ossification, which is essential for therapeutic intervention in heterotopic ossification in AS.
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Registered trials
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