Coronary artery disease (CAD) is the result of atherosclerotic plaque development in the wall of the coronary arteries. The underlying mechanism involves atherosclerosis of the arteries of the heart which is a relatively complex process comprising several steps. In CAD, atherosclerosis induces functional and structural changes. The pathogenesis of CAD results from various changes in and interactions between multiple cell types in the artery walls; these changes mainly include endothelial cell (EC) dysfunction, vascular smooth muscle cell (SMC) alteration, lipid deposition and macrophage activation. Various blood markers associated with an increased risk for cardiovascular endpoints have been identified; however, few have yet been shown to have a diagnostic impact or important clinical implications that would affect patient management. Noncoding RNAs, especially microRNAs (miRNAs) and long noncoding RNAs (lncRNAs), can be stable in plasma and other body fluids and could therefore serve as biomarkers for some diseases. Many studies have shown that some miRNAs and lncRNAs play key roles in heart and vascular development and in cardiac pathophysiology. Thus, we summarize here the latest research progress, focusing on the molecular mechanism of miRNAs and lncRNAs in CAD, with the intent of seeking new targets for the treatment of heart disease.
anti-atherosclerosis by inhibiting the expression of FOXP1 in VSMCs
promote cell proliferation and inhibits apoptosis by inhibiting ZDHHC14 gene expression
suppress cellular migration and vasculogenesis via targeting EGFR
promote aberrant VSMCs proliferation
suppress VEGF expression and EPCs activity
inhibit the expression of adhesion molecules and inflammatory cytokines
regulate inflammatory responses
function as anti-angiogenesis via suppression of AT1R and promote inflammatory signal transduction
anti-inflammatory response by targeting MCP-1
participate in HDL biogenesis
participate in cholesterol synthesis/transport and fatty acid metabolism
regulate cardiac hemostasis and lipid metabolism
regulate cholesterol and fatty-acid metabolism
regulate serum cholesterol level via targeting ABCA1
Serum/ ECs macropahge
regulate cholesterol accumulation by affecting HDL biogenesis
attenuate atherosclerotic lesion by mediating autophagy pathway and regulate cholesterol efflux
regulate thrombocyte activation
govern platelet reactivity
regulate the proliferation and migration of ECs
act as a suppressor of cardiomyocyte autophagy
anti-inflammatory by inhibiting ICAM-1 expression
inhibit pro-inflammatory-induced angiogenesis
influence arterial stiffness through modulating apelin expression
involve in the occurrence of atherosclerosis by regulating TAB3 expression
suppress autophagy process and play an atheroprotective role
stimulate neointimal lesion formation
regulate myocardial ischemia and cardiac remodeling
play a role in VSMCs phenotypic modulation
regulate cell differentiation and promote ECs apoptosis by inhibiting of Bcl-xl
Table 1 Summary of coronary artery disease-related miRNAs.
regulate expression of CDKN2B and modulate VSMCs proliferation
function as a sponge of the let-7 to protect VSMCs
partake in process of atherosclerosis through controlling VSMCs and ECs apoptosis
a novel regulator of neointima formation, vascular smooth muscle cell proliferation, apoptosis, and atherosclerosis by enhancing p53 activity
negatively regulate hypercholesterolemia and inflammatory factor releases, suppress apoptosis of ECs and VSMCs
regulate autophagy in ECs and VSMCs
coregulate in response to Ang II to regulate VSMCs proliferation
stabilize or augment the expression of HAS2 mRNA involved in neointimal hyperplasia and inflammation
remodel of the extracellular matrix and neointimal formation, and inflammation
regulate endothelial differentiation and angiogenesis
regulate endothelial differentiation
promote inflammatory gene transcription in macrophages
negatively regulate let-7e to regulate endothelial function and inflammation
negatively regulate NF-kB expression
promote ABCA1-mediated inflammation and cholesterol efflux in foam cells
regulate cholesterol homeostasis and inflammatory reactions through inhibit NFIA expression
inhibit the expression of APOA1 and the formation of HDL
attenuate the suppression of cell viability and enhancement of cell apoptosis caused by ox-LDL
decrease pro-inflammatory cytokine secretion from THP-1 monocytic cells
regulate the expression of PPARδ to mediate inflammatory response
regulate mitochondrial pathways of oxidative phosphorylation and inflammasome activation
Table 2 Summary of coronary artery disease-related lncRNAs.
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