Functional mechanism and clinical implications of miR-455-5p in delayed fracture healing

  • J Orthop Surg Res. 2025 Oct 29;20(1):943. doi: 10.1186/s13018-025-06365-z.
Yan Ma  #  1 ,  Jinxiang Zhang  #  2  3 ,  Luna He  4 ,  Haitao Xu  5 ,  Xiaolin Zhao  6
Affiliations
  • 1. Department of Orthopaedics, Xishan People's Hospital of Wuxi City, Wuxi, 214000, China.
  • 2. Department of Joint Surgery and Geriatric Orthopedics, The Affiliated Hospital of Youjiang Medical University for Nationalities, Baise, 533000, China.
  • 3. Guangxi Key Laboratory for Preclinical and Translational Research on Bone and Joint Degenerative Diseases, Baise, 533000, China.
  • 4. Department of Respiratory, The First Affiliated Hospital of Chengdu Medical Hospital, Chengdu, 610500, China.
  • 5. Department of Orthopedics, Zhucheng People's Hospital, Weifang, 262200, China.
  • 6. Department of Spine Surgery, Taihe Hospital, Hubei University of Medicine, No.32, Renmin South Road, Shiyan, 442000, China. [email protected].
  • # Contributed equally.
PMID: 41163026 DOI: 10.1186/s13018-025-06365-z
Abstract

Background: Delayed 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.

Method: 208 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.

Results: Serum 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.

Conclusions: miR-455-5p promotes osteogenesis by targeting QKI and shows potential as a biomarker and therapeutic target for DFH.

Keywords
Biomarker; Delayed fracture healing; Osteogenic differentiation; QKI; miR-455-5p.
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