Background/aims: Heart failure is the end result of various kinds of cardiovascular diseases. It has a high rate of morbidity and mortality. This article aims to determine the effect of MeCP2, a key epigenetic regulator, on heart failure.
Methods: The genes associated with heart failure were selected and analyzed using Gene Ontology (GO) term analysis and protein-protein interaction (PPI) network analysis. Significantly up- or downregulated genes in a heart failure animal model were identified, and the genes that had the same or opposite alteration trends as MeCP2 were also recognized. Eighteen hub genes were picked based on topological parameters, and then aberrantly expressed genes with MeCP2 overexpression or knockout were analyzed by GO term, KEGG pathway and PPI analyses.
Results: MeCP2 was downregulated in the heart failure animal model. Through comparison and alignment, 10 dysregulated genes were selected from the 18 hub genes (JAK1, SETD1B, HRC, TTN, LYZ2, TPM3, MYH11, MYH6, ALOX5AP, DECR1). These genes were mainly enriched in cytoskeletal regulation mediated by Rho GTPase and inflammation mediated by chemokine and cytokine signaling pathways.
Conclusions: These dysregulated genes provide a better understanding of the underlying mechanisms of the effect of MeCP2 on heart failure and might be used as targets and prognostic markers of heart failure.
Keywords: Functional enrichment; Heart failure; Mecp2; Protein–protein interactions.
© 2018 The Author(s). Published by S. Karger AG, Basel.