Investigation of shared genetic features and related mechanisms between diabetes and tuberculosis.

ABSTRACT

OBJECTIVE: This study aimed to integrate bioinformatics technology to explore shared hub genes and related mechanisms between diabetes and tuberculosis and to provide a theoretical basis for revealing the disease mechanisms in patients with both diabetes and tuberculosis. METHODS: Differentially expressed genes and Venn analysis were used to identify shared genes between diabetes and tuberculosis. PPI network analysis was used to screen key hub genes. GO and KEGG analyses were used to analyze the potential biological functions of these key hub genes. Immune infiltration analysis was performed using the ssGSEA algorithm. EnrichR online analysis website was used to explore potential therapeutic drugs. RESULTS: The dataset analysis showed that PSMB9, ISG15, RTP4, CXCL10, GBP2, and GBP3 were six hub genes shared by diabetes and tuberculosis, which not only could distinguish between the two disease samples but also had a high diagnostic rate. GO and KEGG analyses showed that these six genes mainly mediate immune-related biological processes such as interferon, interleukin, and chemokine receptor binding, as well as signaling pathways such as RIG-I-like receptor, NOD-like receptor, and proteasome. Immune infiltration analysis showed that high expression of TIL may mediate the development of both diabetes and tuberculosis. In addition, suloctidil HL60 UP, thioridazine HL60 UP, mefloquine HL60 UP, 1-NITROPYRENE CTD 00001569, and chlorophyllin CTD 00000324 were the candidate drugs predicted by this study that were most likely to target hub genes. CONCLUSION: Six differentially expressed genes shared by both diseases (PSMB9, ISG15, RTP4, CXCL10, GBP2, and GBP3) may play a key role in the disease progression of patients with both diabetes and tuberculosis. Candidate drugs targeting these hub genes have therapeutic potential and are worthy of further research. In summary, this study reveals potential shared pathogenic mechanisms between tuberculosis and diabetes.