ArticleJournal of orthopaedic surgery and research2025
The functional mechanism and clinical significance of miR-3651 in the healing process of Pilon fractures.
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.
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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.
- Platelet-rich plasma and stem cell therapies for spondylosis: a systematic review of randomized controlled trials.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2026Review
- Severity-Dependent Contributions of Knee Adduction Moment Lever Arm Components and Associated Gait Variables in Medial Knee Osteoarthritis.Annals of biomedical engineering · 2026Article
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Authors and funding
8 authors.
Funding
Abstract
backgroundPilon fractures are high-energy injuries often associated with delayed healing after treatment. MiR-3651 is a short non-coding RNA, yet its expression level, therapeutic effect, and specific mechanism in the healing process of Pilon fractures remain unclear.
aimThis study investigates the association between miR-3651 expression and Pilon fracture healing, assesses its diagnostic utility, and elucidates its regulatory mechanism.
methodsThe expression levels of miR-3651, KRAS, and osteoclast differentiation markers were detected using RT-qPCR. The diagnostic efficacy of miR-3651 for delayed healing of Pilon fractures was assessed via ROC curve analysis, and logistic regression was employed to identify risk factors influencing delayed healing. Cell viability and apoptosis were measured using the CCK-8 assay and flow cytometry. The targeting relationship between miR-3651 and KRAS was verified through the dual-luciferase reporter assay.
resultsMiR-3651 expression was significantly upregulated in the delayed healing group, with concomitant downregulation of its downstream target KRAS. MiR-3651 effectively distinguished between normal healing and delayed healing and was identified as a risk factor influencing the occurrence of delayed healing. Inhibition of miR-3651 expression reduced osteoclast activity and differentiation while promoting apoptosis; conversely, overexpression of miR-3651 produced the opposite effects. Knockdown of KRAS expression reversed the impact of miR-3651 inhibition on osteoclast activity, apoptosis, and differentiation.
conclusionsDownregulation of miR-3651 expression inhibits osteoclast formation, and knockdown of KRAS restores this inhibitory effect.
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