ArticleJournal of orthopaedic surgery and research2025
Functional mechanism and clinical implications of miR-455-5p in delayed 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. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDelayed fracture healing (DFH) is a common and difficult-to-treat complication after fracture surgery. Early diagnosis serves a key function in clinical management. This research seeks to clarify the molecular mechanism underlying how miR-455-5p modulates osteogenic differentiation via QKI(Quaking), thereby laying a foundation for the early detection and targeted intervention of DFH.
method208 femoral neck fracture patients were divided into NFH (normal fracture healing group, n = 115) and DFH (n = 93) groups. The serum level of miR-455-5p and QKI was measured using qRT-PCR(quantitative reverse transcription-polymerase chain reaction). Pearson correlation analysis was performed to assess the correlation. ROC and logistic regression analyses were performed. In vitro experiments with MC3T3-E1 cells explored its role and target via transfection and dual-luciferase assay.
resultsSerum miR-455-5p was downregulated in DFH (P < 0.01), with diagnostic AUC 0.747, and was an independent risk factor. It increased time-dependently during osteogenic induction. Its inhibition reduced osteogenic markers and suppressed proliferation. QKI has been identified as a target gene of miR-455-5p and exhibits a negative correlation with its expression. The synergistic effect between QKI and miR-455-5p contributes to improved diagnostic performance.
conclusionsmiR-455-5p promotes osteogenesis by targeting QKI and shows potential as a biomarker and therapeutic target for DFH.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.