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Abstract
Atherosclerosis, the leading cause of death in the developed world and nearly the
leading cause in the developing world, is associated with systemic risk factors including
hypertension, smoking, hyperlipidemia, and diabetes mellitus, among others. Nonetheless,
atherosclerosis remains a geometrically focal disease, preferentially affecting the
outer edges of vessel bifurcations. In these predisposed areas, hemodynamic shear
stress, the frictional force acting on the endothelial cell surface as a result of
blood flow, is weaker than in protected regions. Studies have identified hemodynamic
shear stress as an important determinant of endothelial function and phenotype. Arterial-level
shear stress (>15 dyne/cm2) induces endothelial quiescence and an atheroprotective
gene expression profile, while low shear stress (<4 dyne/cm2), which is prevalent
at atherosclerosis-prone sites, stimulates an atherogenic phenotype. The functional
regulation of the endothelium by local hemodynamic shear stress provides a model for
understanding the focal propensity of atherosclerosis in the setting of systemic factors
and may help guide future therapeutic strategies.