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 ri...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.展开更多
高迁移率蛋白A2(high mobility group A2,HMGA2)是一种非组蛋白染色体蛋白,参与转录、分化和胚胎发育等生理过程,同时还与许多人类肿瘤的发生发展密切相关。研究表明HMGA2蛋白过表达与垂体瘤侵袭性、级别和大小等有关。Let-7是microRNA...高迁移率蛋白A2(high mobility group A2,HMGA2)是一种非组蛋白染色体蛋白,参与转录、分化和胚胎发育等生理过程,同时还与许多人类肿瘤的发生发展密切相关。研究表明HMGA2蛋白过表达与垂体瘤侵袭性、级别和大小等有关。Let-7是microRNA家族的成员之一,正常生理情况下其与发育、肌肉形成、细胞粘附和基因调节有关,同时还可以调节细胞周期原癌基因RAS、CDC25a、cyclinD。Let-7缺失或低表达后导致HMGA2过表达,从而引起垂体瘤等多种人类肿瘤发生。本文将对let-7与HMGA2的相互关系及它们对垂体瘤的影响做一综述。展开更多
文摘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.
文摘高迁移率蛋白A2(high mobility group A2,HMGA2)是一种非组蛋白染色体蛋白,参与转录、分化和胚胎发育等生理过程,同时还与许多人类肿瘤的发生发展密切相关。研究表明HMGA2蛋白过表达与垂体瘤侵袭性、级别和大小等有关。Let-7是microRNA家族的成员之一,正常生理情况下其与发育、肌肉形成、细胞粘附和基因调节有关,同时还可以调节细胞周期原癌基因RAS、CDC25a、cyclinD。Let-7缺失或低表达后导致HMGA2过表达,从而引起垂体瘤等多种人类肿瘤发生。本文将对let-7与HMGA2的相互关系及它们对垂体瘤的影响做一综述。
