Potential value of miR-1273f in accelerating the healing of elderly osteoporotic fractures by regulating SFRP4 expression

Objectives This study aimed to investigate the role of miR-1273f in osteoporotic fracture healing by targeting SFRP4, to evaluate its potential as a diagnostic biomarker and therapeutic target. Methods Bioinformatics screening identified miR-1273f as a fracture-related miRNA and SFRP4 as a latent target of miR-1273f. Clinical validation used 144 osteoporosis patients (72 fracture/non-fracture pairs), measuring miR-1273f by RT-qPCR. Human osteoblasts (HObCs) and osteoclasts (HOstCs) were transfected with miR-1273f mimic/inhibitor, or SFRP4 overexpression vector to explore the functions of miR-1273f/SFRP4 axis. Direct targeting was confirmed via dual-luciferase assay. Cell viability was assessed using CCK-8 reagent. Cellular senescence was assessed by flow cytometric quantification of SA-β-Gal-positive cells. Osteoblast migration and osteoclast resorption were analyzed through Transwell and bone resorption kit. Results MiR-1273f was significantly downregulated in osteoporosis patients with fracture compared with unfractured individual and directly suppressed SFRP4 expression. Overexpression of miR-1273f enhanced osteoblast viability, reduced senescence, and promoted migration, while inhibiting osteoclast viability and bone resorption capacity. These effects were reversed by SFRP4 co-expression, confirming their functional interplay. Conclusions This study demonstrates that miR-1273f may accelerate osteoporotic fracture healing by negatively regulating SFRP4, which enhanced osteoblast function while suppressed osteoclast activity. These findings highlight miR-1273f’s dual potential as both a diagnostic biomarker and therapeutic target for age-related bone impairment.