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Abbas, A., Aukrust, P., Russell, D., Krohg-Sorensen, K., Almas, T., Bundgaard, D., et al. (2014) Matrix Metalloproteinase 7 Is Associated with Symptomatic Lesions and Adverse Events in Patients with Carotid Atherosclerosis. PLoS ONE, 9, e84935.
https://doi.org/10.1371/journal.pone.0084935

has been cited by the following article:

  • TITLE: MicroRNA Let-7g and Atherosclerosis Plaque Stabilization

    AUTHORS: Rongping Yin, Chenlin Zhang, Yunying Hou, Xiaohua Wang

    KEYWORDS: Atherosclerosis, Let-7g, MicroRNAs, Plaque, Stabilization

    JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.7 No.2, February 20, 2017

    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.