| Summary: | Clinical and basic research evidence suggests a critical role of local hemodynamic microenvironments in atherogenesis. Disturbed flow with a low and reciprocating shear stress in arterial branches and curvatures induces endothelial dysregulation and damage, leading to atherosclerosis. In contrast, laminar flow with a high and unidirectional shear stress in the straight parts of the arteries elicits an atheroprotective effect on the vasculature. Effective treatment against endothelial dysregulation and the consequent atherogenesis requires the identification of new shear-responsive molecules and the development of drugs targeting these molecules. In this review, we focus on the role of shear-responsive transcription factors and cofactors in endothelial dysfunction and atherosclerosis, and highlight future direction for prevention and treatment of atherosclerosis by targeting these factors.
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