The effect of miR-223-3p on endothelial cells in coronary artery disease.

Endothelial cell damage and dysfunction are crucial factors in the development and early stages of coronary artery disease (CAD) and apoptosis plays a significant role in this process. In this study, We aimed to simulate the CAD vascular microenvironment by treating endothelial cells with tumor necrosis factor alpha (TNF-α) to construct an endothelial cell apoptosis model. Our findings revealed that the TNF-α model resulted in increased micro-RNA 223-3p (miR-223-3p) mRNA and Bax protein expression, decreased kruppel-like factor 15 (KLF15) and Bcl-2 protein expression, and decreased cell viability. More importantly, in the TNF-α-induced endothelial cell apoptosis model, transfection with the miR-223-3p inhibitor reversed the effects of TNF-α on Bcl-2, Bax expression. We transfected miRNA-223-3p mimics or inhibitors into endothelial cells and assessed miR-223-3p levels using RT-PCR. Cell viability was detected using CCK8. Western blot technology was used to detect the expression of Bcl-2, Bax, and KLF15. In summary, this study demonstrates the role and possible mechanism of miR-223-3p in endothelial cells during CAD, suggesting that miR-223-3p may serve as a promising therapeutic target in CAD by regulating KLF15.

Exploring the regulatory roles of circular RNAs in the pathogenesis of atherosclerosis.

Circular RNAs (circRNAs) are a class of noncoding RNAs with a covalently closed loop structure. Recent evidence has shown that circRNAs can regulate gene transcription, alternative splicing, microRNA (miRNA) "molecular sponges", RNA-binding proteins and protein translation. Atherosclerosis is one of the leading causes of death worldwide, and more studies have indicated that circRNAs are related to atherosclerosis pathogenesis, including vascular endothelial cells, vascular smooth muscle cells, inflammation and lipid metabolism. In this review, we systematically summarize the biogenesis, characteristics and functions of circRNAs with a focus on their roles in the pathogenesis of atherosclerosis.