Identification of Biomarkers Associated with Septic Cardiomyopathy Based on Bioinformatics Analyses

被引:13
|
作者
Chen, Mengwei [1 ]
Kong, Chengqi [1 ]
Meng, Zhiyuan [1 ]
Li, Yin [2 ]
机构
[1] Fudan Univ, Huadong Hosp, Dept Cardiovasc, Shanghai, Peoples R China
[2] Fudan Univ, Huadong Hosp, Dept Emergency, Shanghai, Peoples R China
关键词
differentially expressed gene; functional enrichment analysis; protein-protein interaction network; septic cardiomyopathy; SEPSIS; GENES; NORMALIZATION; EXPRESSION; WEBGESTALT; MICRORNAS; SUMMARIES; NETWORKS; DATABASE; MIR-29;
D O I
10.1089/cmb.2019.0181
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
This study intended to identify biomarkers for septic cardiomyopathy (SC). Microarray data GSE79962 including 20 SC samples and 11 normal samples were downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) between SC and control groups were identified, followed with functional enrichment analyses. In addition, the protein-protein interaction (PPI) network and modules were constructed. Finally, a transcription factors (TFs)-microRNA (miRNA)-target gene network was constructed and the potential drugs targeting key DEGs were searched. There were 119 upregulated and 80 downregulated genes in the SC group compared with the control group. The upregulated DEGs were significantly enriched tumor necrosis factor signaling pathway, Jak-signal transducer and activator of transcription (STAT) signaling pathway, hypoxia-inducible transcription factor-1 signaling pathway, chemokine signaling pathway, and cytokine-cytokine receptor interaction. The downregulated genes involved in biological processes of negative regulation of DNA biosynthetic process, and skeletal muscle cell differentiation. CCL2, STAT3, MYC, and SERPINE1 were hub nodes in the PPI network and modules. miR-29 family and miR-30 family were considered as key miRNAs, and TATA, MEF2, and STAT5B were considered as key TFs. SERPINE1 and MYC were also drug target genes. The identified DEGs and pathways may be implicated in the progression of human SC, which may lead to a better understanding of SC pathogenesis.
引用
收藏
页码:69 / 80
页数:12
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