In our study, GO analysis showed that metabolic processes involving nitrogen compounds were up-regulated while the cGMP-PKG signaling pathway was also increased, consistent with a previous study showing decreased NO signaling in endothelial cells and cardiomyocytes, leaded to cardiomyocyte hypertrophy by reducing the activity of soluble guanylate cyclase (sGC) and cyclic guanylate (cGMP) content, as well as cardiomyocyte loss of the protective effects of protein kinase G (PKG) in DCM (Park et al., 2018; Tan et al., 2020). This evidence concerns the gene PRKG1 and familial dilated cardiomyopathy.