Exploring the mechanism and drug candidates of alveolar echinococcosis affecting liver fibrosis through analysis of existing microarray data.

Abstract

Echinococcosis, a zoonotic disease, significantly impacts the liver, with alveolar echinococcosis (AE) often leading to liver fibrosis and, in severe cases, cirrhosis. However, the molecular mechanisms by which AE infection promotes liver fibrosis remain incompletely understood. This study utilized bioinformatic analysis of existing microarray data to explore the shared mechanisms between AE and liver fibrosis and to identify potential therapeutic drug candidates. We analyzed gene expression datasets to identify common differentially expressed genes (DEGs), followed by enrichment analyses using Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes databases to determine biological functions and pathways. A protein-protein interaction network was constructed, and key hub genes were identified using Cytoscape software. Immune cell infiltration was evaluated and correlated with hub gene expression. Transcription factors regulating DEGs were predicted using the TRRUST database, and drug-target interactions were explored using DrugBank. A total of 260 DEGs were identified, primarily associated with cell cycle regulation and immune response pathways. Ten hub genes (DLGAP5, AURKA, MELK, CCNB2, CCNA2, NUF2, BUB1B, BUB1, TOP2A, and CCNB1) were highlighted for their significant interconnectivity and functional relevance. Immune infiltration analysis revealed dysregulation in immune responses, and transcription factor analysis identified E2F3 as a key regulatory factor with decreased expression in both AE and liver fibrosis. Finally, 135 candidate drugs targeting these hub genes were identified, offering new insights into therapeutic strategies. This study provides a foundation for understanding the molecular mechanisms underlying AE-related liver fibrosis and highlights potential drug candidates for clinical exploration.