Experimental Vascular Medicine, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich, Munich, Germany.
Arterioscler Thromb Vasc Biol. 2013 Mar;33(3):449-54. doi: 10.1161/ATVBAHA.112.300279. Epub 2013 Jan 16.
Atherosclerosis is a condition caused by lipid-induced inflammation of the vessel wall orchestrated by a complex interplay of various cell types, such as endothelial cells, smooth muscle cells, and macrophages. MicroRNAs (miRNAs) have emerged as key regulators of gene expression typically by repressing the target mRNA, which determines cell fate and function under homeostatic and disease conditions. Here, we outline the effects of miRNA-145, -126, and -155 in atherosclerosis in vivo. Downregulation of miR-145, which controls differentiation of smooth muscle cells, promotes lesion formation, whereas the endothelial cell-specific miRNA-126 signals the need for endothelial repair through its transfer from apoptotic endothelial cells in microvesicles. Elevated miR-155 levels are characteristic of proinflammatory macrophages and atherosclerotic lesions. However, the effects of miR-155 seem to be different in early and advanced atherosclerosis. The discovery of the role of these miRNAs in atherosclerosis sheds light on the current concepts of atherogenesis and may provide novel treatment options for cardiovascular diseases.
动脉粥样硬化是一种由脂质引起的血管壁炎症引起的疾病，由多种细胞类型（如内皮细胞、平滑肌细胞和巨噬细胞）之间的复杂相互作用所调控。微 RNA（miRNA）已成为基因表达的关键调节因子，通常通过抑制靶 mRNA 来实现，这决定了细胞在稳态和疾病条件下的命运和功能。在这里，我们概述了 miRNA-145、-126 和 -155 在体内动脉粥样硬化中的作用。miR-145 的下调控制平滑肌细胞的分化，促进病变形成，而内皮细胞特异性 miRNA-126 通过其从凋亡内皮细胞的小泡中转移来发出内皮修复的信号。高水平的 miR-155 是促炎巨噬细胞和动脉粥样硬化病变的特征。然而，miR-155 的作用在早期和晚期动脉粥样硬化中似乎不同。这些 miRNA 在动脉粥样硬化中的作用的发现揭示了动脉粥样形成的当前概念，并可能为心血管疾病提供新的治疗选择。
