Mechanistic analysis of abnormal activation of the RANKL-RANK signaling axis in diabetic bone injury

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Objective: Based on bioinformatics analysis methods, this study aims to investigate the mechanism underlying the abnormal activation of the RANKL-RANK signaling axis in diabetic bone injury, as well as its role in the processes of excessive osteoclast differentiation and bone resorption. This work is intended to provide a theoretical basis for mechanistic research and targeted therapy of diabetic osteoporosis. Methods: Transcriptomic data of bone tissue from streptozotocin-induced diabetic C57BL/6J mice and normal control mice were obtained from the GSE189112 dataset in the Gene Expression Omnibus (GEO) database. Differential expression analysis was performed using the limma package, with a threshold of |log2FoldChange| > 0.5 and P < 0.05 to identify differentially expressed genes (DEGs). Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted using the ClusterProfiler package. Results: The osteoclast differentiation pathway was significantly enriched, and key genes, including RANK, IκB, AP1, CTSK, and TRAP, were significantly upregulated, indicating disruption of the RANKL-RANK signaling axis and excessive activation of the downstream NF-κB pathway. Conclusion: The hyperglycemic microenvironment in diabetes promotes osteoclast differentiation by abnormally activating the RANKL-RANK signaling axis, thereby exacerbating bone resorption. This mechanism serves as a crucial molecular basis for diabetic bone loss, and targeting this pathway may hold potential therapeutic value.

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