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MiRNA-mRNA network in osteoporotic fractures proposes the functional mechanism of hsa-miR-32-3p/TNFSF11 axis

Yukai Zeng1,2, Bo Zhao3, Jiawei Gong4

  • 1School of Biomedical Engineering, Capital Medical University, Beijing, 100069, China.

Journal of Orthopaedic Surgery and Research
|April 29, 2025
PubMed
Abstract

Insights

This study reveals that decreased hsa-miR-32-3p and increased TNFSF11 expression in osteoporotic fracture (OF) patients regulate osteoclast activity. The hsa-miR-32-3p/TNFSF11 axis is implicated in OF pathogenesis.

Area of Science:

  • Molecular Biology
  • Genomics
  • Biochemistry

Background:

  • Osteoporotic fracture (OF) is a significant health concern linked to bone metabolism.
  • MicroRNAs (miRNAs) and their mRNA targets play crucial roles in bone remodeling and disease pathogenesis.

Purpose of the Study:

  • To construct a miRNA-mRNA regulatory network in osteoporotic fracture (OF).
  • To investigate the role of the hsa-miR-32-3p/TNFSF11 axis in osteoclast function and OF.

Main Methods:

  • Differential expression analysis of miRNAs using GSE70318 and GSE74209 datasets.
  • Construction of a miRNA-mRNA network and pathway enrichment analysis (GO, KEGG).
  • Validation of the hsa-miR-32-3p/TNFSF11 axis expression and function in osteoclast activity.

Main Results:

  • Identified 21 differentially expressed miRNAs and 36 target genes in OF.
  • The hsa-miR-32-3p/TNFSF11 axis was significantly associated with OF pathogenesis.
  • Decreased hsa-miR-32-3p and increased TNFSF11 expression correlated with low bone mineral density and fracture; hsa-miR-32-3p inhibited osteoclast activation, while TNFSF11 promoted it.

Conclusions:

  • The study established a miRNA-mRNA network implicating TNFSF11 as a target of hsa-miR-32-3p in OF.
  • The hsa-miR-32-3p/TNFSF11 axis is a key regulator of osteoclast activity in the context of osteoporotic fracture.
Keywords:
Hsa-miR-32-3pMiRNAOsteoclastsOsteoporotic fracturesTNFSF11

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