Explore potential biomarkers to provide a theoretical basis for the treatment of liver fibrosis with pirfenidone

Background: Hepatic fibrosis is a common chronic liver disease in clinic, the purpose of our study is to explore potential biomarkers to provide a theoretical basis for the treatment of liver fibrosis with pirfenidone. Methods: We downloaded a gene-sequencing dataset and a single-cell dataset from the GEO database and pirfenidone target genes from three different databases. First, we performed GO, KEGG, and DO analysis on pirfenidone target genes. Then, we grouped the liver tissue sequencing data (GSE162694) in the sequencing data set (N-F0 group and F1-F4 group) and performed gene expression differential analysis on these two groups, weighted gene co-expression network analysis and gene Enrichment analysis. Finally, we intersected the significantly upregulated genes in the F1-F4 group with the pirfenidone target genes and performed PPI network analysis. In order to further explore the expression of both pirfenidone drug target genes and liver fibrosis disease genes (PDLFG) in different immune cells of liver tissue, we used the CD45+ cell data in the GSE136103 data set for further analysis. Results: A subnetwork consisting of CDC42, HNF4A, BHLHE40, CCDC71L, NR1H3, TNF, MGLL, GPT, SCD and PLIN1 was screened out, and by analysis, we finally identified the SCD as PDLFG. In single-cell sequencing analysis, we found that SCD was highly expressed in M2-polarized macrophages. Conclusion : SCD may be an important target protein to inhibit the progression of liver fibrosis.