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Exp Cell Res. 2019 Mar 1;376(1):92-97. doi: 10.1016/j.yexcr.2019.01.005. Epub 2019 Jan 8.

Translocating transcription factors in fluid shear stress-mediated vascular remodeling and disease.

Author information

1
Department of Cell Biology, Yale School of Medicine, United States; Yale Cardiovascular Research Center, United States.
2
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. Electronic address: martin.schwartz@yale.edu.

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.

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