Integrated Analysis of mRNA and lncRNA Expression Profiles Reveals Regulatory Networks Associated with Decompensated Cirrhosis

The stage of decompensation is termed end-stage liver cirrhosis. Patients with decompensated cirrhosis (DCC) often have a variety of comorbidities that contribute to exacerbation of the disease and its high mortality rate. By comparing differential gene expression, transcriptomic analysis is useful for exploring relevant functional changes during disease progression. The purpose of this study was to identify differentially expressed long noncoding RNAs (lncRNAs) and mRNAs in patients with decompensated cirrhosis and to further explore the functions as well as interactions between lncRNAs and mRNAs. Four patients with decompensated cirrhosis and four controls with liver cirrhosis were recruited in this study. RNA was isolated from peripheral blood mononuclear cells, and RNA-seq was used for transcriptome analysis. The functions of differentially expressed mRNAs were revealed by Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, and a regulatory network was also constructed. A total of 1046 differentially expressed mRNAs and 1175 lncRNAs were identified between the decompensated cirrhosis patients and cirrhosis controls. Functional enrichment analyses indicated enrichment of genes involved in pathways related to inflammation and cellular metabolic activities. In addition, the findings suggested that the phagosome/endosome/autophagy-lysosome pathway might play an important role in cirrhotic decompensation. In summary, this study identified differentially expressed mRNAs (DE-mRNAs) and DE-lncRNAs and predicted the biological processes and signaling pathways involved in cirrhotic decompensation, which might provide new ideas for further revealing the molecular mechanism of DCC pathogenesis.

Automated summary

This study identified differentially expressed lncRNAs and mRNAs in patients with decompensated cirrhosis, revealing functional changes and potential pathways involved in the progression of the disease.