28 October 2018 : Laboratory Research
Identification of Potential Gene Interactions in Heart Failure Caused by Idiopathic Dilated Cardiomyopathy
Huijuan Huang1ABCDEF, Beibei Luo1DF, Boqun Wang1C, Qianwen Wu1B, Yuming Liang1F, Yan He1AG*DOI: 10.12659/MSM.912984
Med Sci Monit 2018; 24: LBR7697-7709
Abstract
BACKGROUND: Many heart failure (HF) cases are caused by idiopathic dilated cardiomyopathy (iDCM). This study explored the mechanisms of the development and progression of HF caused by iDCM.
MATERIAL AND METHODS: The gene expression profiles of 102 samples were downloaded from the GEO database (GSE5406). Differentially expressed genes (DEGs) were identified through GO analysis and a KEGG pathway analysis, respectively. A protein–protein interaction (PPI) network was constructed and analyzed to screen potential regulatory proteins. In addition, MCODE and a cytoHubba plugin were used to identify the module and hub genes of DEGs. Finally, transcription factors (TFs) were predicted using PASTAA. We did not perform whole-exome sequencing (WES) for detecting mitochondrial DNA (mtDNA).
RESULTS: A total of 197 DEGs were screened, and 3 modules, and 4 upregulated and 11 downregulated hub genes were screened. The GO analysis focused on the terms and 12 KEGG pathways were enriched. The FOS, TIMP1, and SERPINE1 hub genes, as well as some key TFs, demonstrated important roles in the progression of HF caused by iDCM. CEBPD, CEBOB, CDC37L1, and SRGN may be new targets for HF in iDCM patients.
CONCLUSIONS: The identified DEGs and their enriched pathways provide references for exploring the mechanisms of the development and progression of HF patients with iDCM. Moreover, modules, hub genes, and TFs may be useful in the treatment and diagnosis of HF patients with iDCM. However, mtDNA was not investigated.
Editorial
01 October 2024 : Editorial
Editorial: Potentials and Pitfalls in Targeting Glucagon-Like Peptide-1 (GLP-1) in the Management of Increasing Levels of ObesityDOI: 10.12659/MSM.946675
Med Sci Monit 2024; 30:e946675
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