Identification of potential candidate genes and dysregulated mechanisms of heart failure

Background Heart failure (HF) adversely affects quality of life. This work aims to increase the understanding of the biology of HF in order to identify candidate markers that can provide the most effective diagnosis and treatment. Methods Gene expression profiles in HF and non-failing (NF) samples were collected from GSE116250 and GSE141910. Differentially expressed genes (DEGs) between HF and NF were identified, and common genes were obtained using intersection analysis. Enrichment analysis was performed to identify biological mechanisms underlying HF. Further, candidate genes were screened using the least absolute shrinkage and selection operator (LASSO) analysis. The diagnostic role of candidate genes to predict the occurrence of HF was evaluated by meta-analysis and ROC curves. In addition, we also utilized xCell to analyze the differences in immune cell infiltration between HF and NF. Results A total of 379 common genes were obtained as differentially expressed between HF and NF. Enrichment analysis identified common genes mainly involved in the immune response, Toll-like receptor signaling pathway. Through the LASSO model, we identified eight candidate genes (PHLDA1, C1QTNF2, SPC24, FNDC1, FREM1, SLC16A9, PLA2G2A, and S1PR3). The meta-analysis and ROC curves results suggest that the candidate genes are highly sensitive for the diagnosis of HF. Finally, we found that neutrophil, B cell plasma, and Th1 CD4 + T cell were significantly infiltrated in HF. Conclusion To identify potential diagnostic and therapeutic candidate genes using gene expression profiling of HF patients. In the future, more efforts are needed to investigate the role of candidate genes in HF.