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ORIGINAL RESEARCH article
Front. Genet.
Sec. Computational Genomics
Volume 16 - 2025 | doi: 10.3389/fgene.2025.1559798
This article is part of the Research Topic Advances in circRNA Research: Disease Associations and Diagnostic Innovations View all articles
Comprehensive Analysis of Non-Coding RNA-Mediated Endothelial Cell-Specific Regulatory Circuits in Coronary Artery Disease Risk
Provisionally accepted
Boshui Huang 1* Zhijie Lai 2* Xiaoyu Wang 3* Qinhao Zhang 4* Tingting Hu 4* Fulong Yu 4*
Shuxian Zhou 1
Yan Zhang 3* Juan Meng 5*- 1 Department of Cardiology, Sun Yat-sen Memorial Hospital, Guangzhou, China
- 2 Division of Cardiology, Puning People's Hospital, Puning, China, Puning, China
- 3 Guangdong Provincial People's Hospital, Guangzhou, Guangdong Province, China
- 4 School of Life Sciences, Guangzhou University, Guandong, China
- 5 State Key Discipline of Infection Diseases, Shenzhen Third People's Hospital, Shenzhen, China
Coronary artery disease (CAD) remains the leading cause of mortality worldwide, driven by both lifestyle factors and genetic predisposition. Large-scale population genetic studies have greatly enhanced our understanding of the genetic underpinnings of CAD and facilitated the discovery of disease-associated genes. Noncoding RNAs, such as circular RNAs (circRNAs) and microRNAs (miRNAs), play crucial roles in the regulation of these genes. However, the impact of CAD-associated genetic variants on noncoding RNAs and their regulatory gene networks remain largely unexplored. In this study, we systematically identified the targets of both noncoding and coding genes influenced by CAD-associated variants. We constructed a CAD risk gene network, encompassing circRNAs, miRNA and genes, based on the concept of competing endogenous RNA regulation. Additionally, we focused on the endothelial cell (EC)-specific gene regulatory network to prioritize diseaseassociated circRNAs. Notably, we identified two CAD-associated variants that may disrupt circZNF609 and circABCC1, potentially altering their function as miRNA sponges and impacting EC-specific gene regulation, ultimately contributing to disease risk. Our findings link CAD genetic predisposition to noncoding RNA-mediated gene regulatory mechanisms in specific cell types, providing a valuable resource for novel target identification and advancing precision medicine in CAD.
Keywords: Coronary artery disease (CAD), Circular RNA (circRNA), GWAS, Endothelial cell (EC), genetic variants
Received: 13 Jan 2025; Accepted: 07 Feb 2025.
Copyright: © 2025 Huang, Lai, Wang, Zhang, Hu, Yu, Zhou, Zhang and Meng. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Boshui Huang, Department of Cardiology, Sun Yat-sen Memorial Hospital, Guangzhou, 510000, China
Zhijie Lai, Division of Cardiology, Puning People's Hospital, Puning, China, Puning, China
Xiaoyu Wang, Guangdong Provincial People's Hospital, Guangzhou, 510317, Guangdong Province, China
Qinhao Zhang, School of Life Sciences, Guangzhou University, Guandong, China
Tingting Hu, School of Life Sciences, Guangzhou University, Guandong, China
Fulong Yu, School of Life Sciences, Guangzhou University, Guandong, China
Yan Zhang, Guangdong Provincial People's Hospital, Guangzhou, 510317, Guangdong Province, China
Juan Meng, State Key Discipline of Infection Diseases, Shenzhen Third People's Hospital, Shenzhen, China
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