Abstract
Despite increased public health awareness, atherosclerosis remains a leading cause of mortality worldwide. Significant variations in response to statin treatment have been noted among different populations suggesting that the efficacy of statins may be altered by both genetic and environmental factors. The existing literature suggests that certain long noncoding RNAs (lncRNAs) might be up- or downregulated among patients with atherosclerosis. LncRNA may act on multiple levels (cholesterol homeostasis, vascular inflammation, and plaque destabilization) and exert atheroprotective or atherogenic effects. To date, only a few studies have investigated the interplay between statins and lncRNAs known to be implicated in atherosclerosis. The current review characterizes the role of lncRNAs in atherosclerosis and summarizes the available evidence related to the effect of statins in regulating lncRNAs.
Highlights
Atherosclerosis is a chronic, progressive disease characterized by the hardening and thickening of the arterial wall and the formation of plaques that consist of immune and mesenchymal cells, lipids, and extracellular matrix [1]
The present review aims to characterize the current knowledge regarding long noncoding RNAs (lncRNAs) implicated in the process of atherosclerosis as well as summarize the available evidence related to the effect of statins in regulating lncRNAs
Considering that lncRNAs are emerging as essential mechanisms involved in lipid metabolism and play an important role in controlling transcriptional and post-transcriptional regulatory pathways, lncRNAs represent meaningful candidates to help predict response to statin treatment and explain the variations in treatment response
Summary
Atherosclerosis is a chronic, progressive disease characterized by the hardening and thickening of the arterial wall and the formation of plaques that consist of immune and mesenchymal cells, lipids, and extracellular matrix [1]. Not all patients will achieve physiological cholesterol levels after high-intensity statin treatment [5]. Numerous lncRNAs have been implicated in certain atherogenic processes, including endothelial dysfunction, lipid deposition, and inflammation [9,10,11,12]. Significant progress has been made in characterizing lncRNAs that are implicated in atherosclerosis, it is estimated that fewer than 5% have been identified to date. Still not completely understood, there is evidence to suggest that statins may exert their pleiotropic effects by regulating certain lncRNAs. The present review aims to characterize the current knowledge regarding lncRNAs implicated in the process of atherosclerosis as well as summarize the available evidence related to the effect of statins in regulating lncRNAs
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