Conclusion
CTRL, ARHGEF5, PPAP2C, VSIG2, and PBLD show high potential as molecular targets for basic and clinical research in osteoclast-mediated OP.
Discussion
Currently, there are no studies on the effects of these five genes on osteoclast differentiation. Therefore, it is meaningful to design in vivo and in vitro perturbation experiments to observe the impact of each gene on osteoclast differentiation and OP progression. Conclusion: CTRL, ARHGEF5, PPAP2C, VSIG2, and PBLD show high potential as molecular targets for basic and clinical research in osteoclast-mediated OP.
Methods
Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were performed on the OP patient datasets from the GEO database. The
Objective
The pathological mechanism of osteoporosis (OP) involves increased bone resorption mediated by osteoclasts and decreased bone formation mediated by osteoblasts, leading to an imbalance in bone homeostasis. Identifying key molecules in osteoclast-mediated OP progression is crucial for the prevention and treatment of OP.
Results
CTRL, ARHGEF5, PPAP2C, VSIG2, and PBLD were identified as key genes. These genes exhibited strong disease relevance (AUC > 0.9). Functional enrichment results also indicated their close association with OP and osteoclast differentiation. In vitro differential expression validation showed that during osteoclast differentiation, CTRL was downregulated, while ARHGEF5, PPAP2C, VSIG2, and PBLD were upregulated, with all differences being statistically significant (P < 0.05).