ArticleJournal of orthopaedic surgery and research2025
The role and regulatory mechanism of miR-122-5p in the process of pilon fracture healing.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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Who cites it
2 citing papers in PubMed.
- The functional mechanism and clinical significance of miR-3651 in the healing process of Pilon fractures.Journal of orthopaedic surgery and research · 2025Article
- Management Strategies for Failed Pilon Fractures: A Personalized Approach to Revision Reconstruction.Journal of personalized medicine · 2025Review
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Authors and funding
4 authors.
Funding
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Abstract
objectiveTo explore the role and mechanism of miR-122-5p in the process of fracture healing following a Pilon fracture, as well as to further assess the clinical significance of this molecule as a potential diagnostic marker for fracture nonunion.
methodsThe expression levels of miR-122-5p were examined in patients with Pilon fracture healed and nonunion, respectively. ROC analysis was employed to evaluate the diagnostic value of miR-122-5p in identifying fracture nonunion, while logistic regression identified its risk factors. The effects of miR-122-5p on the proliferation, apoptosis, and osteogenic differentiation markers of osteoblasts were analyzed by CCK-8 assays, flow cytometry, RT-qPCR, and ALP assay kit. Additionally, DLR and RIP assays validated miR-122-5p targeting PDCD4.
resultsSerum miR-122-5p was significantly under-expressed in patients with fracture nonunion, whereas PDCD4 exhibits a notable over-expressed. Serum miR-122-5p can predict non-union of fractures, with a sensitivity of 90.82% and a specificity of 78.33%. Low miR-122-5p expression is a potential risk factor for fracture nonunion. The overexpression of miR-122-5p enhanced the proliferation ability of osteoblasts, inhibited cell apoptosis, and upregulated the expressions of ALP, OCN, and RUNX2; knockdown of miR-122-5p elicits opposite effect. PDCD4 is a direct target of miR-122-5p. The osteoblast dysfunction induced by miR-122-5p inhibitors can be reversed by down-regulating PDCD4.
conclusionDiminished miR-122-5p emerge as a potential prognostic indicator for nonunion in Pilon fractures. miR-122-5p accelerates the healing of Pilon fractures by targeting and inhibiting PDCD4.
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