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.

Highlights

  • Coronary artery disease (CAD) is a common disorder caused by atherosclerotic processes in the coronary arteries

  • Atherosclerosis is regarded as a progressive inflammatory condition during which oxidative, hemodynamic, and biochemical factors destruct the function of endothelial cells [2]

  • We summarize the function of long non-coding RNAs (lncRNAs) and circRNAs in the development and progression of CAD

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Summary

INTRODUCTION

Coronary artery disease (CAD) is a common disorder caused by atherosclerotic processes in the coronary arteries. Two classes of regulatory non-coding RNAs, namely, long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs), have been shown to affect the process of atherosclerosis and CAD development [5, 6] Both having regulatory effects on the expression of genes, they vary in terms of biogenesis and mechanism of action. Overexpression of NEXN-AS1 suppressed TLR4 oligomerization and nuclear factor κB (NF-κB) function, decreased endothelial production of adhesion proteins and inflammatory cytokines, and repressed adhesion of monocyte to endothelial cells [17]. LncRNAs Alter Function of Endothelial Cells and Vascular Smooth Muscle Cells ANRIL is another up-regulated lncRNA in CAD patients as well as animal model of this disorder.

15 CAD tissues and HUVECs
20 CAD tissues and Endothelial cell miR-9-3p
DISCUSSION

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