LAUSR

Background Biliary atresia (BA) is an uncommon illness that causes the bile ducts outside and within the liver to become clogged in babies. If left untreated, the cholestasis causes increasing conjugated hyperbilirubinemia, cirrhosis, and hepatic failure. BA has a complicated aetiology, and the mechanisms that drive its development are unknown. The objective of this study was to show the role of probable critical genes involved in the pathophysiology of biliary atresia. Methods We utilised the public Gene Expression Omnibus (GEO) microarray expression profiling dataset GSE46960 to find differentially expressed genes (DEGs) in 64 biliary atresia newborns, 14 infants with various causes of intrahepatic cholestasis, and 7 deceased-donor children as control subjects in our study. The relevant information was looked into. The important modules were identified after functional enrichment, GO and KEGG pathway analyses, protein-protein interaction (PPI) network analyses, and GSEA analysis. Results The differential expression analysis revealed a total of 22 elevated genes. To further understand the biological activities of the DEGs, we run functional enrichment analyses on them. Meanwhile, KEGG analysis has revealed significant enrichment of pathways involved in activating cross-talking with inflammation and fibrosis in BA. SERPINE1, THBS1, CCL2, MMP7, CXCL8, EPCAM, VCAN, ITGA2, AREG, and HAS2, which may play a significant regulatory role in the pathogenesis of BA, were identified by PPI studies. Conclusion Our findings suggested 10 hub genes and probable mechanisms of BA in the current study through bioinformatic analysis.