Integrated Bioinformatics Analysis Identifies Key Gene Markers and Pathways in Irritable Bowel Syndrome with Diarrhea
نویسندگان
1 Department of Gastroenterology, The Affiliated Hospital of Xuzhou Medical University, 221002 Xuzhou, Jiangsu, China
2 Department of Gastroenterology, Xuzhou Medical University, 221002 Xuzhou, Jiangsu, China
3 Department of Gastroenterology, Xuzhou Medical University, 221002 Xuzhou, Jiangsu, China
doi
10.22034/ircmj.2025.506077.1875چکیده
Background and Objectives: The pathogenesis of irritable bowel syndrome with diarrhea (IBS-D) is not fully clear. This study aims to explore the underlying disease mechanisms of IBS-D using bioinformatics approaches. Methods: Raw sequencing data related to IBS-D were downloaded from the GEO database (datasets GSE14841, GSE36701, GSE146853, and GSE166869), followed by differential gene expression analysis using R. Disease-related genes associated with IBS-D were identified from five databases: Genecards, Disgenet, TTD, Drugbank, and OMIM. Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, and protein-protein interaction (PPI) analysis were performed on the identified genes. Further disease correlation analysis of key genes was conducted using the Comparative Toxicogenomics Database (CTD). Results: A total of 481 differentially expressed genes (305 upregulated, 176 downregulated) were identified from the GEO datasets. Enrichment analysis suggested that the pathogenesis of IBS-D may involve multiple molecular mechanisms, including immune response, chromatin remodeling, and viral infections. Across the disease databases, 228 IBS-D-related genes were found (Genecards: 222, Drugbank: 6). GEO dataset and the disease database had a total of 4 intersecting genes (CCL2, MUC1, CASR, PRKCA). Related disease analysis of the key 4 genes by CTD database revealed that IBS-D was associated with Chemical and Drug Induced Liver Injury, Fatty Liver, Hepatomegaly, Liver Cirrhosis, Liver Diseases, Liver Neoplasms existed in correlation. Conclusion: CCL2, MUC1, CASR and PRKCA may be involved in the pathological process of IBS-D through IL-17 signaling pathway and bile secretion regulation, and their co-occurrence with liver diseases in the CTD database suggests that the mechanism of intestinal-hepatic interactions is worth exploring in depth.