Hu Xiaofeng, Shen Guilin, Lu Xiaoli, Ding Guomin, Shen Lishui
Department of Cardiology, Zhejiang Hospital, Hangzhou, Zhejiang Province, China.
Department of Cardiology, Anji People's Hospital, Huzhou, Zhejiang Province, China.
Arch Med Sci. 2019 Mar;15(2):484-497. doi: 10.5114/aoms.2018.75593. Epub 2018 May 4.
Hypertrophic cardiomyopathy (HCM), a genetically heterogeneous disorder of cardiac myocytes, is one of the main causes of sudden cardiac death of young people. However, the molecular mechanism involved in HCM has remained largely unclear. Of note, non-coding RNAs were reported to play an important role in human diseases. In this study, we focused on identifying differentially expressed long non-coding RNA (lncRNAs) and mRNAs in HCM by analyzing a public dataset (GSE36961).
We performed bioinformatics analysis to explore key pathways underlying HCM progression. Gene Ontology (GO) analysis was first performed to evaluate the potential roles of differentially expressed genes and lncRNAs in HCM. Moreover, protein-protein interaction (PPI) networks were constructed to reveal interactions among differentially expressed proteins. Specifically, co-expression networks were also constructed to identify hub lncRNAs in HCM.
A total of 6147 mRNAs ( < 0.001) and 126 lncRNAs ( < 0.001) were found to be dysregulated in HCM. Gene Ontology (GO) analysis showed that these differentially expressed genes and lncRNAs were associated with metabolism, energy pathways, signal transduction, and cell communication. Moreover, TSPYL3, LOC401431, LOC158376, LOC606724, PDIA3P and LOH3CR2A ( < 0.001) were identified as key lncRNAs in HCM progression.
Taken together, our analysis revealed a series of lncRNAs and mRNAs that were differentially expressed in HCM and which were involved in HCM progression by regulating pathways, such as metabolism, energy pathways, signal transduction, and cell communication. This study will provide useful information to explore the mechanisms underlying HCM progression and to provide potential candidate biomarkers for diagnosis in HCM.
肥厚型心肌病（HCM）是一种心肌细胞的基因异质性疾病，是年轻人心脏性猝死的主要原因之一。然而，HCM所涉及的分子机制在很大程度上仍不清楚。值得注意的是，据报道非编码RNA在人类疾病中起重要作用。在本研究中，我们通过分析一个公共数据集（GSE36961），着重于鉴定HCM中差异表达的长链非编码RNA（lncRNA）和信使核糖核酸（mRNA）。
我们进行了生物信息学分析，以探索HCM进展的关键途径。首先进行基因本体论（GO）分析，以评估差异表达基因和lncRNA在HCM中的潜在作用。此外，构建蛋白质-蛋白质相互作用（PPI）网络以揭示差异表达蛋白质之间的相互作用。具体而言，还构建了共表达网络以鉴定HCM中的枢纽lncRNA。
共发现6147个mRNA（<0.001）和126个lncRNA（<0.001）在HCM中表达失调。基因本体论（GO）分析表明，这些差异表达的基因和lncRNA与代谢、能量途径、信号转导和细胞通讯有关。此外，TSPYL3、LOC401431、LOC158376、LOC606724、PDIA3P和LOH3CR2A（<0.001）被鉴定为HCM进展中的关键lncRNA。
综上所述，我们的分析揭示了一系列在HCM中差异表达的lncRNA和mRNA，它们通过调节代谢、能量途径、信号转导和细胞通讯等途径参与HCM进展。本研究将为探索HCM进展的机制以及为HCM诊断提供潜在的候选生物标志物提供有用信息。
