In the cardiovascular system, the flow of blood within the complex vascular network creates hemodynamic shear forces experienced by cells. Situated between the circulating blood and the bulk vascular tissue, the endothelium is a cell monolayer acting as a barrier that protects the underlying arterial tissue. Shear forces have been seen to interact with and regulate endothelial cells through mechanotransduction induced cytoskeletal changes within the cell [1]. Shear forces can be beneficial in cases of laminar flow, which are thought to be atheroprotective by aligning and organizing endothelial cells [2]. However, disturbances to a smooth flow field, caused by vessel bifurcations or obstructions like an implanted stent or a bulging atherosclerotic lesion, can cause recirculation zones to form downstream. In these flow regions, detrimental monolayer remodeling occurs which breaks down the endothelial barrier function [3]. Biochemically, it has been seen that shear forces drive signaling cascades in the Rho/Rac pathways that cascade into morphological changes in the cytoskeleton [4].

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