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

Jialing Wang; Pengtao Li; Yuqian Li; Chunsheng Wang; Kulaixi Xilizhati; Jianrong Ye

doi:10.1016/j.actatropica.2025.107532

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

Acta Trop. 2025 Jan 23:107532. doi: 10.1016/j.actatropica.2025.107532. Online ahead of print.

Authors

Jialing Wang¹, Pengtao Li², Yuqian Li³, Chunsheng Wang³, Kulaixi Xilizhati³, Jianrong Ye⁴

Affiliations

¹ Department of Department of Anesthesiology, the First Affiliated Hospital of Xinjiang Medical University, No. 137, South Liyushan Road, Xinshi District, Urumqi, Xinjiang, 830054, China; Xinjiang Perioperative Organ Protection Laboratory, No. 137, South Liyushan Road, Xinshi District, Urumqi, Xinjiang, 830054, China.
² Department of Neurosurgery, Peking Union Medical College Hospital, Peking Union Medical College, Chinese Academy of Medical Sciences, No.1 Shuaifuyuan, Dongcheng District, Beijing, 100730, China.
³ Department of Department of Anesthesiology, the First Affiliated Hospital of Xinjiang Medical University, No. 137, South Liyushan Road, Xinshi District, Urumqi, Xinjiang, 830054, China.
⁴ Department of Department of Anesthesiology, the First Affiliated Hospital of Xinjiang Medical University, No. 137, South Liyushan Road, Xinshi District, Urumqi, Xinjiang, 830054, China; Xinjiang Perioperative Organ Protection Laboratory, No. 137, South Liyushan Road, Xinshi District, Urumqi, Xinjiang, 830054, China. Electronic address: yejianrong1978@163.com.

PMID: 39863141
DOI: 10.1016/j.actatropica.2025.107532

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.

Keywords: Alveolar echinococcosis; Drug candidates; Liver fibrosis; Mechanism.