Inhibition of miR-224-5p promotes osteogenesis in dental pulp stem cells by targeting the PTEN/PI3K/AKT axis
Ke Z., Yang F., Huang N., Lv H.
Laboratory Study on Face & Skin, published in J Orthop Surg Res (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
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- Study type
- Laboratory Study
- Journal
- J Orthop Surg Res (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41965804
- PMCID
- PMC13270850
- DOI
- 10.1186/s13018-026-06853-w
Abstract (original English)
Background MiR-224-5p has been proven to play an important role in regulating cell differentiation. This study aimed to clarify the regulatory role and mechanism of miR-224-5p in the osteogenic differentiation of human dental pulp stem cells (hDPSCs), thereby laying a theoretical foundation for subsequent jaw defect repair. Methods Human dental pulp stem cells (hDPSCs) were isolated, cultured, and sorted from healthy dental pulp tissues. We performed integrated bioinformatics analysis to screen and identify the potential targets and pathways of miR-224-5p involved in the osteogenic induction of hDPSCs. Subsequently, in vitro experiments were conducted. Plasmid transfection was used to regulate the overexpression and knockdown of miR-224-5p in hDPSCs, and the expression of osteogenesis-related proteins was detected. Furthermore, luciferase reporter assays and Western blot assays were used to confirm the direct targets of miR-224-5p, and rescue experiments were performed to verify the underlying mechanism. Results The results demonstrated that overexpression of miR-224-5p inhibited the osteogenic differentiation of DPSCs, as reflected by the significantly decreased expression of osteogenic markers (OCN, Runx2, and ALP). In contrast, inhibition of miR-224-5p promoted the osteogenic differentiation of DPSCs. Bioinformatics analysis and dual-luciferase reporter gene assays indicated
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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