ArticleStem cell research & therapy2025
Inhibition of miR-615-3p enhances dentinogenesis in scap
Article in Stem cell research & therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
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
3 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
- SSUH2 Promotes Odontogenic Differentiation of SCAPs via the FOXM1/PDK1-Mediated Regulation of Mitochondrial Function.International endodontic journal · 2026Article
- Dysregulation of miR-140-3p is involved in the pathogenesis of pulpitis via the regulation of ACSL1.Odontology · 2026Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
backgroundMesenchymal stem cells (MSCs) are critical for dental tissue regeneration, yet their differentiation potential is tightly regulated by microRNAs (miRNAs). This study aimed to investigate the role of miR-615-3p in regulating odontogenic differentiation in stem cells from the apical papilla (SCAPs), offering insights into potential applications for enhancing dental tissue regeneration and repair.
methodsQuantitative PCR (qPCR), Western blot analysis, alkaline phosphatase (ALP) activity assay, and Alizarin Red staining (ARS) were performed to assess odontogenic differentiation following miR-615-3p modulation in SCAPs. Mitochondrial function was evaluated by measuring reactive oxygen species (ROS) levels, membrane potential, and respiratory activity. In vivo, SCAPs with miR-615-3p modulation were transplanted into rabbit extraction sockets to examine dentin-like tissue formation.
resultsmiR-615-3p was significantly downregulated in SCAPs compared to umbilical cord mesenchymal stem cells (WJCMSCs) and further decreased during mineralization induction, suggesting its negative regulatory role in odontogenic differentiation. Inhibition of miR-615-3p enhanced ALP activity, mineralization, and odontogenic marker expression both in vitro and in vivo. Proteomic analysis revealed that miR-615-3p inhibition improved mitochondrial function by reducing ROS levels and increasing mitochondrial function. Further Competing Endogenous RNA Sequencing(ceRNA-seq) analysis identified PVT1 as a downstream target of miR-615-3p. PVT1 overexpression promoted odontogenic differentiation and mitochondrial homeostasis, while its knockdown impaired these processes. Collectively, the miR-615-3p/PVT1 axis emerged as a critical regulator of dentinogenesis through mitochondrial modulation.
conclusionsInhibiting miR-615-3p fosters dentinogenesis through PVT1-mediated mitochondrial regulation in SCAPs. These findings highlight the miR-615-3p/PVT1 axis as a promising target for enhancing dentin tissue engineering applications.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.