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High shear stress induces atherosclerotic vulnerable plaque formation through angiogenesis

机译:高剪切应力通过血管生成诱导动脉粥样硬化易损斑块形成

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摘要

Rupture of atherosclerotic plaques causing thrombosis is the main cause of acute coronary syndrome and ischemic strokes. Inhibition of thrombosis is one of the important tasks developing biomedical materials such as intravascular stents and vascular grafts. Shear stress (SS) influences the formation and development of atherosclerosis. The current review focuses on the vulnerable plaques observed in the high shear stress (HSS) regions, which localizes at the proximal region of the plaque intruding into the lumen. The vascular outward remodelling occurs in the HSS region for vascular compensation and that angiogenesis is a critical factor for HSS which induces atherosclerotic vulnerable plaque formation. These results greatly challenge the established belief that low shear stress is important for expansive remodelling, which provides a new perspective for preventing the transition of stable plaques to high-risk atherosclerotic lesions.
机译:引起血栓形成的动脉粥样硬化斑块破裂是急性冠状动脉综合征和缺血性中风的主要原因。抑制血栓形成是开发生物医学材料(如血管内支架和血管移植物)的重要任务之一。剪切应力(SS)影响动脉粥样硬化的形成和发展。目前的评论集中在高剪切应力(HSS)区域中观察到的易损斑块,该区域位于侵入腔腔的斑块的近端区域。血管向外重塑发生在HSS区域以进行血管补偿,并且血管生成是HSS的关键因素,HSS诱导动脉粥样硬化易损斑块形成。这些结果极大地挑战了已确立的信念,即低剪切应力对于扩大重塑很重要,这为防止稳定斑块过渡到高危动脉粥样硬化病变提供了新的视角。

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