Prognosis of extracorporeal membrane oxygenation (ECMO) treatment on cardiogenic shock after acute myocardial infarction: a retrospective bioinformatics analysis
Chuanzhen Liu, Weisong Li, Shuqin LiuBackground:
Cardiogenic shock after acute myocardial infarction (AMI) becomes more common with age and the improvement of living standards. Extracorporeal membrane oxygenation (ECMO) is an effective treatment for such patients. However, genes and molecular processes that can predict the prognosis of shock after AMI with ECMO treatment are not known.
Methods:
The microarray dataset (GSE93101, n = 14) was retrieved from the Gene Expression Omnibus online database. Differential expression, weighted gene co-expression network analyses (WGCNA), Gene Ontology, and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed. To identify the top five hub genes, we used the mutual construction of the protein–protein interaction network and the Cytoscape software. Subsequently, a gene–microRNA (miRNA) network was established to identify the miRNAs that potentially regulate these hub genes.
Results:
Ten genes were obtained when those in the two highest correlation modules of WGCNA were intersected with the differentially expressed genes. A total of 104 differentially expressed genes were found to be associated with oxidoreductase activity and metabolic pathways. We found the top five hub genes using the Cytoscape software: CD68, C8A, NR1H4, and ADGRE1 genes were downregulated, while TMPRSS6 was upregulated. TMPRSS6 had the highest degree of affinity and was regulated by 29 miRNAs, while CD68, NR1H4, CD163, and C8A were regulated by 18, 14, 14, and 2 miRNAs, respectively. Although CD163 was not in the top five hub genes, it is regulated by more miRNAs.
Conclusion:
Through comprehensive analysis, CD68, which was regulated by 18 miRNAs, emerged as a promising prognostic biomarker for ECMO after AMI, and the mechanism may reflect macrophage activation and differentiation, thereby modulating postinfarction inflammatory responses and tissue repair.