Abstract
We designed this study to identify potential key protein interaction networks, genes, and correlated pathways in dilated cardiomyopathy (DCM) via bioinformatics methods. We selected the GSE3586 microarray dataset, consisting of 15 dilated cardiomyopathic heart biopsy samples and 13 nonfailing heart biopsy samples. Initially, the GSE3586 dataset was downloaded and was analyzed with the limma package to identify differentially expressed genes (DEGs). A total of 172 DEGs consisting of 162 upregulated genes and ten downregulated genes in DCM were selected by the criterion of adjusted Pvalues less than 0.01 and the log2-fold change of 0.6 or greater. Gene Ontology functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were performed to view the biological processes, cellular components, molecular function, and KEGG pathways of the DEGs. Next, protein-protein interactions were constructed, and the hub protein modules were identified. Then we selected the key genes DLD, UQCRC2, DLAT, SUCLA2, ATP5A1, PRDX3, FH, SDHD, and NDUFV1, which are involved in a wide range of biological activities, such as the citrate cycle, oxidation-reduction processes and cellular respiration, and energy derivation by oxidation of organic compounds in mitochondria. Finally, we found that currently there are no related gene-targeting drugs after exploring the predicted interactions between key genes and drugs, and transcription factors. In conclusion, our study provides greater understanding of the pathogenesis and underlying molecular mechanisms in DCM. This contributes to the exploration of potential gene therapy targets.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.