BACKGROUND: Osteoporosis is a significant public health issue worldwide. The underlying mechanism of osteoporosis is an imbalance between bone resorption and bone formation. However, the exact pathology is still unclear, and more related genes are on demand. AIM: Here, we aim to identify the differentially expressed genes in osteoporosis patients and control. MATERIALS AND METHODS: Biblio-MetReS, a tool to reconstruct gene and protein networks from automated literature analysis, was used for identifying potential interactions among target genes. Relevant signaling pathways were also identified through pathway enrichment analysis. RESULTS: Our results showed that 56 differentially expressed genes were identified. Of them, STAT1, CXCL10, SOCS3, ADM, THBS1, SOD2, and ERG2 have been demonstrated involving in osteoporosis. Further, a bibliometric network was constructed between DEGs and other genes through the Biblio-MetReS. CONCLUSIONS: The results showed that STAT1 could interact with CXCL10 through Toll-like receptor signaling pathway and Chemokine signaling pathway. STAT1 interacted with SOCS3 through JAK/STAT pathway.
BACKGROUND:Osteoporosis is a significant public health issue worldwide. The underlying mechanism of osteoporosis is an imbalance between bone resorption and bone formation. However, the exact pathology is still unclear, and more related genes are on demand. AIM: Here, we aim to identify the differentially expressed genes in osteoporosispatients and control. MATERIALS AND METHODS: Biblio-MetReS, a tool to reconstruct gene and protein networks from automated literature analysis, was used for identifying potential interactions among target genes. Relevant signaling pathways were also identified through pathway enrichment analysis. RESULTS: Our results showed that 56 differentially expressed genes were identified. Of them, STAT1, CXCL10, SOCS3, ADM, THBS1, SOD2, and ERG2 have been demonstrated involving in osteoporosis. Further, a bibliometric network was constructed between DEGs and other genes through the Biblio-MetReS. CONCLUSIONS: The results showed that STAT1 could interact with CXCL10 through Toll-like receptor signaling pathway and Chemokine signaling pathway. STAT1 interacted with SOCS3 through JAK/STAT pathway.