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Updated: Nov 13, 2025

In Silico Identification and Characterization of circRNAs During Host-Pathogen Interactions
Published on: October 21, 2022
The Emerging Role of Long Non-coding RNAs and Circular RNAs in Coronary Artery Disease
Soudeh Ghafouri-Fard1, Mahdi Gholipour2, Mohammad Taheri3
1Urogenital Stem Cell Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Insights
Long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) play key roles in coronary artery disease (CAD) development. This review details their specific functions and involvement in CAD pathogenesis.
Area of Science:
- Cardiovascular Biology
- Molecular Genetics
- RNA Biology
Background:
- Coronary artery disease (CAD) stems from atherosclerosis, involving complex cellular interactions within artery walls.
- Key factors include lipid accumulation, endothelial dysfunction, macrophage activation, and smooth muscle cell alterations.
- Emerging evidence highlights the role of non-coding RNAs in CAD pathogenesis.
Purpose of the Study:
- To review the involvement of long non-coding RNAs (lncRNAs) in CAD.
- To summarize the role of circular RNAs (circRNAs) in CAD.
- To consolidate current understanding of ncRNA function in CAD development and progression.
Main Methods:
- Literature review of studies on lncRNAs and circRNAs in CAD.
- Analysis of gene expression data from CAD patients.
- Examination of functional studies on specific lncRNAs and circRNAs.
Main Results:
- Several lncRNAs (e.g., H19, ANRIL, MIAT) are upregulated in CAD patients.
- Other lncRNAs (e.g., Gas5, MEG3) are downregulated in CAD patients.
- Specific circRNAs impact endothelial and smooth muscle cell functions, contributing to CAD.
Conclusions:
- lncRNAs and circRNAs are significant contributors to CAD pathogenesis.
- Dysregulation of these non-coding RNAs is a hallmark of CAD.
- Understanding ncRNA roles offers potential therapeutic targets for CAD.
Abstract:
Coronary artery disease (CAD) is a common disorder caused by atherosclerotic processes in the coronary arteries. This condition results from abnormal interactions between numerous cell types in the artery walls. The main participating factors in this process are accumulation of lipid deposits, endothelial cell dysfunction, macrophage induction, and changes in smooth muscle cells. Several lines of evidence underscore participation of long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs) in the pathogenesis of CAD. Several lncRNAs such as H19, ANRIL, MIAT, lnc-DC, IFNG-AS1, and LEF1-AS1 have been shown to be up-regulated in the biological materials obtained from CAD patients. On the other hand, Gas5, Chast, HULC, DICER1-AS1, and MEG3 have been down-regulated in CAD patients. Meanwhile, a number of circRNAs have been demonstrated to influence function of endothelial cells or vascular smooth muscle cells, thus contributing to the pathogenesis of CAD. In the current review, we summarize the function of lncRNAs and circRNAs in the development and progression of CAD.
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