MiR-148a-3p regulates the fracture healing process by targeting MAFB
MiR-148a-3p regulates the fracture healing process by targeting MAFB

MiR-148a-3p regulates the fracture healing process by targeting MAFB

J Orthop Surg Res. 2025 Sep 24;20(1):826. doi: 10.1186/s13018-025-06223-y.

ABSTRACT

BACKGROUND: Osteoporotic vertebral fracture (OVF) is an extremely common fragile fracture in the elderly population.

AIMS: To explore the expression changes, clinical significance and mechanism of action of miR-148a-3p in the postoperative healing process of patients with OVF.

METHODS: 185 OVF patients who received percutaneous vertebroplasty (PVP) treatment were selected as the research subjects. RT-qPCR was used to detect the expression levels of miR-148a-3p and genes. ROC curve analysis was applied to evaluate the relationship between miR-148a-3p and postoperative healing, as well as its diagnostic value for delayed healing. In vitro, miR-148a-3p overexpression and knockdown cell models were established to investigate its potential mechanism in fracture healing.

RESULTS: Serum miR-148a-3p expression in OVF patients was significantly higher than in healthy controls, and it gradually decreased over time after surgery. The expression of miR-148a-3p in the delayed healing group is significantly higher than that in the healing group, and it showed potential diagnostic value for delayed healing (AUC = 0.859). In addition, miR-148a-3p is an independent risk factor for delayed healing. In cell experiments, during the process of osteogenic induction, expression of miR-148a-3p decreased, while the expression of osteogenic markers increased. Mechanistically, miR-148a-3p directly targeted and inhibited MAFB expression; its upregulation suppressed cell proliferation and osteogenic marker expression, and these inhibitory effects were reversed by MAFB overexpression.

CONCLUSIONS: miR-148a-3p inhibits osteoblast proliferation and differentiation by targeting and suppressing MAFB, participates in the post-OVF healing process.

PMID:40993742 | DOI:10.1186/s13018-025-06223-y