Weighted gene co-expression network analysis reveals similarities and differences of molecular features between dilated and ischemic cardiomyopathies

Felix K. Biwott, Ni-Ni Rao, Chang-Long Dong, Guang-Bin Wang
{"title":"Weighted gene co-expression network analysis reveals similarities and differences of molecular features between dilated and ischemic cardiomyopathies","authors":"Felix K. Biwott,&nbsp;Ni-Ni Rao,&nbsp;Chang-Long Dong,&nbsp;Guang-Bin Wang","doi":"10.1016/j.jnlest.2023.100193","DOIUrl":null,"url":null,"abstract":"<div><p>Cardiomyopathies represent the most common clinical and genetic heterogeneous group of diseases that affect the heart function. Though progress has been made to elucidate the process, molecular mechanisms of different classes of cardiomyopathies remain elusive. This paper aims to describe the similarities and differences in molecular features of dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM). We firstly detected the co-expressed modules using the weighted gene co-expression network analysis (WGCNA). Significant modules associated with DCM/ICM were identified by the Pearson correlation coefficient (PCC) between the modules and the phenotype of DCM/ICM. The differentially expressed genes in the modules were selected to perform functional enrichment. The potential transcription factors (TFs) prediction was conducted for transcription regulation of hub genes. Apoptosis and cardiac conduction were perturbed in DCM and ICM, respectively. TFs demonstrated that the biomarkers and the transcription regulations in DCM and ICM were different, which helps make more accurate discrimination between them at molecular levels. In conclusion, comprehensive analyses of the molecular features may advance our understanding of DCM and ICM causes and progression. Thus, this understanding may promote the development of innovative diagnoses and treatments.</p></div>","PeriodicalId":53467,"journal":{"name":"Journal of Electronic Science and Technology","volume":"21 2","pages":"Article 100193"},"PeriodicalIF":0.0000,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Electronic Science and Technology","FirstCategoryId":"95","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1674862X23000113","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"Engineering","Score":null,"Total":0}
引用次数: 0

Abstract

Cardiomyopathies represent the most common clinical and genetic heterogeneous group of diseases that affect the heart function. Though progress has been made to elucidate the process, molecular mechanisms of different classes of cardiomyopathies remain elusive. This paper aims to describe the similarities and differences in molecular features of dilated cardiomyopathy (DCM) and ischemic cardiomyopathy (ICM). We firstly detected the co-expressed modules using the weighted gene co-expression network analysis (WGCNA). Significant modules associated with DCM/ICM were identified by the Pearson correlation coefficient (PCC) between the modules and the phenotype of DCM/ICM. The differentially expressed genes in the modules were selected to perform functional enrichment. The potential transcription factors (TFs) prediction was conducted for transcription regulation of hub genes. Apoptosis and cardiac conduction were perturbed in DCM and ICM, respectively. TFs demonstrated that the biomarkers and the transcription regulations in DCM and ICM were different, which helps make more accurate discrimination between them at molecular levels. In conclusion, comprehensive analyses of the molecular features may advance our understanding of DCM and ICM causes and progression. Thus, this understanding may promote the development of innovative diagnoses and treatments.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
加权基因共表达网络分析揭示了扩张型和缺血性心肌病分子特征的异同
心肌病是影响心功能的最常见的临床和遗传异质性疾病。虽然在阐明这一过程方面取得了进展,但不同类型心肌病的分子机制仍然难以捉摸。本文旨在描述扩张型心肌病(DCM)和缺血性心肌病(ICM)分子特征的异同。我们首先使用加权基因共表达网络分析(WGCNA)检测共表达模块。通过模块与DCM/ICM表型之间的Pearson相关系数(PCC)鉴定与DCM/ICM相关的显著模块。选择模块中差异表达的基因进行功能富集。对枢纽基因的转录调控进行了潜在转录因子(TFs)预测。在DCM和ICM中,细胞凋亡和心脏传导分别受到干扰。TFs表明DCM和ICM的生物标志物和转录调控不同,这有助于在分子水平上更准确地区分它们。综上所述,全面分析DCM和ICM的分子特征有助于我们了解DCM和ICM的病因和进展。因此,这种认识可能会促进创新诊断和治疗的发展。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Journal of Electronic Science and Technology
Journal of Electronic Science and Technology Engineering-Electrical and Electronic Engineering
CiteScore
4.30
自引率
0.00%
发文量
1362
审稿时长
99 days
期刊介绍: JEST (International) covers the state-of-the-art achievements in electronic science and technology, including the most highlight areas: ¨ Communication Technology ¨ Computer Science and Information Technology ¨ Information and Network Security ¨ Bioelectronics and Biomedicine ¨ Neural Networks and Intelligent Systems ¨ Electronic Systems and Array Processing ¨ Optoelectronic and Photonic Technologies ¨ Electronic Materials and Devices ¨ Sensing and Measurement ¨ Signal Processing and Image Processing JEST (International) is dedicated to building an open, high-level academic journal supported by researchers, professionals, and academicians. The Journal has been fully indexed by Ei INSPEC and has published, with great honor, the contributions from more than 20 countries and regions in the world.
期刊最新文献
Source localization based on field signatures: Laboratory ultrasonic validation Machine learning model based on non-convex penalized huberized-SVM Iterative physical optics method based on efficient occlusion judgment with bounding volume hierarchy technology A multi-scale persistent spatiotemporal transformer for long-term urban traffic flow prediction Big data challenge for monitoring quality in higher education institutions using business intelligence dashboards
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1