Abstract
Vascular atherosclerotic vulnerable plaque rupture is the primary cause of acute myocardial infarctions and strokes. Thus, stabilization of vulnerable plaques is of important clinical endeavor to decrease the fatal risk of atherosclerosis. Inflammatory infiltration, apoptosis of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), destruction of extracellular matrix (ECM) or collagen, and neovascularization all contribute to the formation and stability of plaque. Let-7g, one miRNA of let-7 family, is related to retardation of the progress of vulnerable atherosclerosis plaque. First of all, let-7g induced preservation on vascular diseases through regulating on the intracellular Ca2+- activated protein kinase C-oxLDL-LOX-1 pathway, which resulted in reduced leukocyte adhesion to and migration across endothelium. Over expression of let-7g negatively regulated apoptosis in the ECs by targeting lectin-like oxidized LDL receptor-1(LOX-1)/CASP3 expression, therefore made the fibrous cap of plaque integrated and thick, increased the density of vascular atherosclerotic plaque. In addition, let-7g might stabilize the atherosclerotic plaque through other aspects. In this review, we focus on current and potential importance of let-7g on the stabilization of atherosclerosis plaque which might lead to the future development of an alternative strategy of CAD.
Highlights
Vascular atherosclerotic plaque rupture is the major cause of acute myocardial infarctions and strokes [1]
Inflammatory infiltration, apoptosis of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs), destruction of extracellular matrix (ECM) or collagen, and neovascularization all contribute to the formation and stability of plaque
We focus on current and potential importance of let-7g on the stabilization of atherosclerosis plaque which might lead to the future development of an alternative strategy of CAD
Summary
Vascular atherosclerotic plaque rupture is the major cause of acute myocardial infarctions and strokes [1]. Various intrinsic and extrinsic factors influence the stability of plaques, resulting in lifethreatening complications. Those factors include, but not limit to, continuous inflammatory responses, matrix degradation, and cell death or apoptosis. These changes lead to thinner fibrous cap and prone to rupture. MicroRNAs (miRNAs), a kind of noncoding RNA, are one of the largest gene families [5] They have been indicated intargeting around 60% of human genes and regulated a range of biological processes, such as TGF-β and SIRT-1 signaling, Fas/FasL apoptotic pathways, and NF-κB pathway [6]. MiRNAs are associated with apoptosis, cell maturation, oxidative stress, degradation of extracellular matrix (ECM), angiogenesis, and inflammation [7] [8] [9] [10]
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