在流体切应力介导的血管重塑和疾病中易位转录因子。
Translocating transcription factors in fluid shear stress-mediated vascular remodeling and disease.
机构信息
Department of Cell Biology, Yale School of Medicine, United States; Yale Cardiovascular Research Center, United States.
Department of Cell Biology, Yale School of Medicine, United States; Yale Cardiovascular Research Center, United States; Department of Medicine (Cardiology), United States; Department of Biomedical Engineering, United States.
出版信息
Exp Cell Res. 2019 Mar 1;376(1):92-97. doi: 10.1016/j.yexcr.2019.01.005. Epub 2019 Jan 8.
Abstract
Endothelial cells are exposed to fluid shear stress profiles that vary in magnitude, pulsatility, and directionality due to regional variations in blood vessel structure. Laminar flow at physiological levels is atheroprotective; multidirectional or reversing low (disturbed) flow promotes inflammation and disease; and high or low laminar flow promote outward or inward remodeling, respectively. However, our understanding of how endothelial cells discern these different flow profiles and regulate gene expression accordingly is limited. This article reviews recent studies that identify the TGFβ/Smad, Notch, Yap/Taz, and Wnt/β-catenin pathways as important mediators of flow profile- and magnitude-dependent signaling.
摘要
内皮细胞暴露于流体力剪切应力谱中，这些剪切应力谱的大小、脉动性和方向性因血管结构的区域变化而变化。生理水平的层流具有抗动脉粥样硬化作用；多方向或反向低流（紊乱流）促进炎症和疾病；而高或低层流分别促进向外或向内重塑。然而，我们对于内皮细胞如何辨别这些不同的流动模式并相应地调节基因表达的理解是有限的。本文综述了最近的研究，这些研究确定了 TGFβ/Smad、Notch、Yap/Taz 和 Wnt/β-catenin 途径作为流动模式和幅度依赖性信号的重要介质。
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