Dhawan Saurabh S, Avati Nanjundappa Ravi P, Branch Jonathan R, Taylor W Robert, Quyyumi Arshed A, Jo Hanjoong, McDaniel Michael C, Suo Jin, Giddens Don, Samady Habib
Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA 30322, USA.
Expert Rev Cardiovasc Ther. 2010 Apr;8(4):545-56. doi: 10.1586/erc.10.28.
Although traditional cardiovascular risk factors 'prime the soil' for atherogenesis systemically, atherosclerosis primarily occurs in a site-specific manner with a predilection towards the inner wall of curvatures and outer wall of bifurcations with sparing of flow-dividers. Wall shear stress is a frictional force exerted parallel to the vessel wall that leads to alteration of the endothelial phenotype, endothelial cell signaling, gene and protein expression leading to a proinflammatory phenotype, reduced nitric oxide availability and disruption of the extracellular matrix, which in turn leads to plaque development. Clinical and experimental data are emerging that suggest the pathobiology associated with abnormal wall shear stress results in atherosclerotic plaque development and progression.
尽管传统的心血管危险因素会在全身范围内为动脉粥样硬化的发生“准备土壤”，但动脉粥样硬化主要以位点特异性的方式发生，倾向于发生在曲率内壁和分叉外壁，而分流器部位则不受影响。壁面剪应力是一种平行于血管壁施加的摩擦力，它会导致内皮细胞表型改变、内皮细胞信号传导、基因和蛋白质表达改变，从而导致促炎表型、一氧化氮可用性降低以及细胞外基质破坏，进而导致斑块形成。越来越多的临床和实验数据表明，与异常壁面剪应力相关的病理生物学过程会导致动脉粥样硬化斑块的形成和进展。
