ArticleJournal of orthopaedic surgery and research2026
Inhibition of miR-224-5p promotes osteogenesis in dental pulp stem cells by targeting the PTEN/PI3K/AKT axis.
Article in Journal of orthopaedic surgery and research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
Abstract
backgroundMiR-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.
methodsHuman 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.
resultsThe 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 that miR-224-5p specifically targets the 3' untranslated region of the PTEN gene. Rescue experiments further confirmed that miR-224-5p regulates this process by modulating the PTEN/PI3K/AKT pathway.
conclusionsInhibition of miR-224-5p promotes osteogenesis in DPSCs by targeting the PTEN/PI3K/AKT signaling axis. These findings provide reliable evidence for the fabrication of three-dimensional tissue-engineered structures and further repair of maxillofacial bone defects.
Indexed as
Identifiers
What Socratic holds
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.