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Blood vessels are continually below the influence of hemodynamic forces including: 1) shear strain, which can be the tangential frictional force acting around the vessel wall due to blood flow, defined as force/wall location (e.g., dyn/cm2); 2) hydrostatic stress, the perpendicular force acting on the vascular wall; and 3) cyclic strain, the circumferential stretch from the vessel wall (Figure 1A) [1]. As an interface among the blood flow and vessel wall, endothelial cells (ECs) is exposed to these hemodynamic forces. Certainly, it is actually nicely established that the signaling arising from EC-blood flow interaction are essential determinants of vascular homeostasis. ECs and neighboring smooth muscle cells (SMC) are also involved in signaling communication, the net outcome of which influences vascular remodeling, myogenic tone and vascular response to vasoactive agonists.Substantial research over the past handful of decades have showed that vascular ECs sense mechanical force and transduce them into biological responses [2-5], termed as mechanotransduction. This complex method entails perturbation of sensors that generate biochemical signals that initiate complicated and mul.