Shear stress and plaque development.
Shear stress and plaque development.
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DOI：
10.1586/erc.10.28
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发表时间：
2010-04
影响因子：
2
通讯作者：
Samady H
中科院分区：
文献类型：
--
作者：
Dhawan SS;Avati Nanjundappa RP;Branch JR;Taylor WR;Quyyumi AA;Jo H;McDaniel MC;Suo J;Giddens D;Samady H
尽管传统的心血管危险因素系统性地为动脉粥样硬化提供了“土壤”，但动脉粥样硬化主要以特定部位的方式发生，倾向于弯曲的内壁和分叉的外壁，而血流分隔器则不受影响。壁剪切应力是一种平行于血管壁施加的摩擦力，导致内皮表型、内皮细胞信号、基因和蛋白质表达的改变，导致促炎表型、一氧化氮可用性降低和细胞外基质的破坏，进而导致斑块的形成。临床和实验数据表明，与异常壁剪切应力相关的病理生物学导致动脉粥样硬化斑块的发展和进展。
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.