Atherosclerosis, the leading cause of death in the Western world and nearly the leading cause in other developing countries, is associated with systemic risk factors such as hypertension, smoking, diabetes mellitus, and hyperlipidemia (Malek et al., 1999a). Nonetheless, it is clearly a focal disease with atherosclerotic lesions forming in the coronary arteries, major branches of the aortic arch, and the abdominal aorta. Plaque formation preferentially involves the outer walls of vessel bifurcations and points of blood flow recirculation, where hemodynamic shear stress is weaker than in unaffected areas. Detailed analysis of fluid mechanics in these areas revealed a strong spatial correlation between endothelial dysfunction/plaque formation and low mean shear stress and oscillatory flow with recirculation (Nerem, 1992; Malek et al., 1999a). It has been suggested that low mean shear stress and nonlaminar flow stimulate the formation of an atherogenic phenotype (Gibson et al., 1993; Ku et al., 1985) while arterial level shear stress (≥15 dynes/cm2) stimulates atheroprotective gene expression profile and cellular responses that are essential for normal endothelial function (Harrison, 2005; Cunningham and Gotlieb, 2005), implying that the maintenance of physiological, laminar shear stress on endothelial cells is crucial for normal vascular function (Traub and Berk, 1998). The development of atherogenesis can be studied at various levels; however, the origins of the disease have been linked to mechanosensing by a number of studies (Ku et al., 1985; Glagov et al., 1988; Svindland, 1983; Debakey et al., 1985; White et al., 2003), suggesting that investigations at the molecular level are required for further understanding of the atherogenesis.