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Vascular endothelial responses to altered shear stress: pathologic implications for atherosclerosis.

机译:血管内皮对改变的切应力的反应:动脉粥样硬化的病理学意义。

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Atherosclerosis preferentially develops at branches and curvatures of the arterial tree, where blood flow is disturbed from a laminar pattern, and wall shear stress is non-uniform and has an irregular distribution. Vascular endothelial cells (ECs), which form an interface between the flowing blood and the vessel wall, are exposed to blood flow-induced shear stress. There is increasing evidence suggesting that laminar blood flow and sustained high shear stress modulate the expression of EC genes and proteins that function to protect against atherosclerosis; in contrast, disturbed blood flow and the associated low and reciprocating shear stress upregulate proatherosclerotic genes and proteins that promote development of atherosclerosis. Understanding of the effects of shear stress on ECs will provide mechanistic insights into its role in the pathogenesis of atherosclerosis. The aim of this review article is to summarize current findings on the effects of shear stress on ECs, in terms of their signal transduction, gene expression, structure, and function. These endothelial cellular responses have important relevance to understanding the pathophysiological effects of altered shear stress associated with atherosclerosis and thrombosis and their complications.
机译:动脉粥样硬化优先发生在动脉树的分支和弯曲处,那里的血流受到层流模式的干扰,壁切应力不均匀且分布不规则。在流动的血液和血管壁之间形成界面的血管内皮细胞(EC)暴露于血流引起的切应力。越来越多的证据表明,层流和持续的高剪切应力会调节EC基因和蛋白的表达,从而起到预防动脉粥样硬化的作用。相反,血液流动紊乱以及相关的低和往复剪切应力会上调促进动脉粥样硬化发展的前动脉粥样硬化基因和蛋白质。了解剪切应力对EC的影响,将提供有关其在动脉粥样硬化发病机理中作用的机制的见解。本文的目的是就剪切应力对EC的信号转导,基因表达,结构和功能方面的最新发现进行总结。这些内皮细胞反应与理解与动脉粥样硬化和血栓形成及其并发症相关的剪切应力改变的病理生理效应具有重要的关联。

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