Common molecular basis for MASH and hepatitis C revealed via systems biology approach

• DOI: 10.3389/fonc.2024.1442221
• Publication Date: 2024-11-04T12:37:49Z
• Authors: Yongwei Cheng; Zihao Song; Ye Liu; Xichao Xu; Dali Zhang; Yigui Zou; Liang Liu; Yinzhen Zeng; Wenwen Li; Daming Bai; Dongling Dai
• Keywords: Hepatitis C; Steatohepatitis; Liver disease; STAT2

Background Metabolic dysfunction-associated steatohepatitis (MASH) is characterized by liver inflammation and damage caused a buildup of fat in the liver. Hepatitis C, hepatitis C virus (HCV), disease that can lead to cirrhosis, cancer, failure. MASH are common causes cirrhosis hepatocellular carcinoma. Several studies have shown hepatic steatosis also histological feature HCV infected patients. However, molecular basis for remains poorly understood. Methods Firstly, differentially expressed genes (DEGs) were extracted from GSE89632, GSE164760 GSE14323 datasets. Subsequently, DEGs shared among these datasets determined using Venn diagram. Next, protein-protein interaction (PPI) network was constructed based on hub extracted. Then, gene ontology (GO) pathway analysis performed. Furthermore, transcription factors (TFs) miRNAs regulatory networks constructed, drug candidates identified. After cell model treated with predicted drug, expression levels signature measured qRT-PCR ELISA. Results 866 identified C. The GO showed most significantly enriched biological process positive regulation cytokine production. 10 genes, including STAT1, CCL2, ITGAM, PTPRC, CXCL9, IL15, SELL, VCAM1, TLR4 CCL5, selected PPI network. By constructing TF-gene miRNA-gene network, prominent TFs screened out. Potential drugs screening shows Budesonide Dinoprostone may benefit patients, cellular experiments effectively inhibited related glycolipid metabolism, fibrosis, inflammatory factors. Conclusion We between performed series analyses genes. Molecular docking vitro revealed suppress progression This study provide novel insights into potential targets biomarkers