ArticleCellular and molecular life sciences : CMLS2025
Mechanistic insights into miR-584-5p-mediated Inhibition of PDLSCs osteogenic differentiation through H2AFZ upregulation and RUNX2 suppression.
Article in Cellular and molecular life sciences : CMLS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
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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.
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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
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- The Role of MicroRNA in the Behaviour of Periodontal Ligament Stem Cells and Stem Cells from the Apical Papilla: A Systematic Review.Stem cell reviews and reports · 2026Pooled it
- miR-584-5p alleviates osteoarthritis by targeting HIF1A to regulate chondrocyte function and extracellular matrix metabolism.Journal of orthopaedic surgery and research · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Periodontal ligament stem cells (PDLSCs) hold promise for bone regeneration, but their osteogenic differentiation is tightly regulated by various molecular mechanisms. MicroRNAs are key regulators of this process, and miR-584-5p has been identified as a potential modulator of osteogenesis. In this study, we investigated the role of miR-584-5p in the osteogenic differentiation of PDLSCs. Our findings show that overexpression of miR-584-5p inhibits osteogenic differentiation in vitro, as evidenced by reduced alkaline phosphatase activity, diminished mineralized nodule formation, and decreased expression of osteogenic markers, including ALPL, SP7, and RUNX2. In animal models, suppression of miR-584-5p enhances bone formation in both ectopic bone formation and rat calvarial defect models. Mechanistically, we demonstrate that miR-584-5p upregulates the histone variant H2AFZ, leading to its increased nuclear localization and binding to osteogenic gene promoters, including ALPL, SP7, and RUNX2, thereby repressing their expression. Furthermore, miR-584-5p directly targets RUNX2 mRNA, further suppressing its expression. Rescue experiments confirmed that knockdown of H2AFZ or overexpression of RUNX2 mitigates the suppressive effects of miR-584-5p on osteogenesis. Our study reveals that miR-584-5p inhibits osteogenic differentiation of PDLSCs through dual mechanisms: H2AFZ upregulation and RUNX2 suppression, offering novel insights into the epigenetic regulation of bone formation and potential therapeutic strategies for bone regeneration.
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Registered trials
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