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特发性扩张型心肌病所致心力衰竭的潜在基因相互作用鉴定。

Identification of Potential Gene Interactions in Heart Failure Caused by Idiopathic Dilated Cardiomyopathy.

机构信息

Department of Geriatric Cardiology, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China (mainland).

出版信息

Med Sci Monit. 2018 Oct 28;24:7697-7709. doi: 10.12659/MSM.912984.

DOI:10.12659/MSM.912984
PMID:30368515
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6216482/
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.

摘要

背景

许多心力衰竭(HF)病例是由特发性扩张型心肌病(iDCM)引起的。本研究探讨了 iDCM 引起的 HF 发展和进展的机制。

材料和方法

从 GEO 数据库(GSE5406)下载了 102 个样本的基因表达谱。通过 GO 分析和 KEGG 途径分析分别鉴定差异表达基因(DEGs)。构建和分析蛋白质-蛋白质相互作用(PPI)网络,筛选潜在的调节蛋白。此外,使用 MCODE 和 cytoHubba 插件识别 DEGs 的模块和枢纽基因。最后,使用 PASTAA 预测转录因子(TFs)。我们没有进行全外显子组测序(WES)来检测线粒体 DNA(mtDNA)。

结果

筛选出 197 个差异表达基因,筛选出 3 个模块,4 个上调和 11 个下调的枢纽基因。GO 分析主要集中在术语和 12 个 KEGG 途径上进行了富集。FOS、TIMP1 和 SERPINE1 枢纽基因以及一些关键的 TFs 在 iDCM 引起的 HF 进展中发挥了重要作用。CEBPD、CEBOB、CDC37L1 和 SRGN 可能是 iDCM 患者 HF 的新靶点。

结论

鉴定的 DEGs 及其富集途径为探讨 iDCM 患者 HF 发展和进展的机制提供了参考。此外,模块、枢纽基因和 TFs 可能对 iDCM 患者 HF 的治疗和诊断有用。但是,没有研究 mtDNA。

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