Diagnostic Potential of Circulating lncRNA SNHG5 in Osteoporotic Fractures and Its Mechanistic Role in Accelerating...

This study aimed to investigate the diagnostic value of lncRNA SNHG5 in osteoporotic fractures (OPF) and its molecular mechanism in promoting fracture healing.

A total of 120 patients with OPF and 126 patients with OP were included in this study. The expression levels of SNHG5, miR-23a-3p, RUNX2, ALP, OCN, and OPN were detected by RT-qPCR. The diagnostic value of SNHG5 was assessed by ROC curve analysis. CCK-8 assay and flow cytometry were used to detect cell proliferation and apoptosis. The targeting relationship between SNHG5 and miR-23a-3p was predicted by bioinformatics and verified by dual luciferase reporter assay.

SNHG5 was significantly downregulated in OPF patients, particularly in those with delayed healing. Elevated SNHG5 downregulated miR-23a-3p and concurrently increased the expression of osteogenic differentiation-related genes (RUNX2, ALP, OCN, and OPN) in MC3T3-E1 cells. In addition, SNHG5 promotes osteoblast proliferation and inhibits apoptosis. Mechanistically, SNHG5 is directly targeted by miR-23a-3p, which inhibits SNHG5-mediated effects on osteoblasts.

SNHG5 indirectly enhances osteoblast activity by negatively regulating miR-23a-3p, thereby promoting fracture healing. Our study could furnish both theoretical and experimental support for the discovery of innovative treatment targets.