细胞间通讯和器官串扰中的MicroRNA胞外囊泡偷渡。

M. Rogers, E. Aikawa
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引用次数: 5

摘要

细胞外囊泡(EVs)作为细胞间通讯和器官串扰的介质,但对这一关键通讯过程在心血管和相关疾病中所起的机制作用尚缺乏完整的了解。在正常情况下,EV串扰对正常的细胞和器官功能是重要的,但在病变情况下,EV货物可以以促进疾病病理的方式改变。在电动汽车中已经观察到多种货物,包括rna,如microRNA、DNA、蛋白质和脂质,它们可以被包裹在电动汽车内或与电动汽车膜相关。鉴于这一关键功能,确定ev在正常生理和疾病驱动机制中的通讯作用具有很大的治疗前景。在这一期的《动脉硬化、血栓形成和血管生物学》中,Chang等人3提出EV转运是miR-92a从内皮细胞转运到巨噬细胞的主要途径,进而促进动脉粥样硬化的发展。本研究确定了miR-92a细胞-细胞通讯如何在动脉粥样硬化血管中发生的关键机制,并提高了ev相关的miR-92a作为疾病生物标志物和治疗靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
MicroRNA Extracellular Vesicle Stowaways in Cell-Cell Communication and Organ Crosstalk.
Extracellular vesicles (EVs) function as mediators of cell-cell communication1 and organ crosstalk,2 but a complete understanding of the mechanistic roles this critical communication process plays in cardiovascular and associated diseases is lacking. In normal conditions, EV crosstalk is important for proper cell and organ function, but in diseased conditions EV cargos can be altered in a way that promotes disease pathology. Multiple cargos have been observed in EVs, including RNAs, such as microRNA, DNA, proteins, and lipids, which can be encased within EVs or associated with EV membranes. Given this critical function, identifying the communication roles of EVs in normal physiology and diseasedriving mechanisms holds great therapeutic promise. In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology, Chang et al3 propose EV transport as a major pathway in which miR-92a is transported from endothelial cells to macrophages that, in turn, contributes to the development of atherosclerosis. This study identifies a key mechanism of how miR-92a cell-cell communication occurs in atherosclerotic vasculature and raises the potential of EV-associated miR-92a as a disease biomarker and therapeutic target.
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