A system biology approach to determine therapeutic targets by identifying molecular mechanisms and key pathways for type 2 diabetes that are linked to the development of tuberculosis and rheumatoid arthritis.

AIMS: Due to traditional endocrinological techniques, there is currently no shared work available, and no therapeutic choices have been presented in type 2 diabetes (T2D), rheumatoid arthritis (RA), and tuberculosis (TB). The purpose of this research is to summarize the prospective molecular complications and potential therapeutic targets associated with T2D that have been connected to the development of TB and RA.

MATERIALS AND

METHODS

We collected the transcriptomic data as GSE92724, GSE110999 and GSE 148036 for T2D, RA and TB patients. After collecting from NCBI, then GREIN were employed to process our datasets. STRING and Enrichr were used to construct protein-protein interaction (PPI), gene regulatory network (GRN), protein-drug-chemical, gene ontology and pathway network. Finally, Cytoscape and R studio were employed to visualize our proposed network.

KEY FINDINGS: We discovered a number of strong candidate hub proteins in significant pathways, namely RAB25, MAL2, SFN, MYO5B, and HLA-DQB1 out of 75 common genes. We also identified a number of TFs (JUN, TFAP2A, FOXC1, and GATA2); miRNA (mir-1-3p, mir-16-5p, and mir-34a5p); drugs (sulfasalazine, cholic acid, and nilflumic acid) and chemicals (Valproic acid, and Aflatoxin B1) may control DEGs in transcription as well as post- transcriptional expression levels.

SIGNIFICANCE: To summarize, our computational techniques discovered unique potential biomarkers that show how T2D, RA, and TB interacted, as well as pathways and gene regulators by which T2D may influence autoimmune inflammation and infectious diseases. In the future, more clinical and pharmacological research is needed to confirm the findings at the transcriptional and translational levels.