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动脉粥样硬化有压力:生物力学应激与动脉粥样硬化。

Atheromas feel the pressure: biomechanical stress and atherosclerosis.

机构信息

Vanderbilt University School of Medicine, Department of Pathology, 1161 21 Ave. South. C2217A MCN, Nashville, TN 37232, USA.

出版信息

Am J Pathol. 2010 Jul;177(1):4-9. doi: 10.2353/ajpath.2010.090615. Epub 2010 Jun 17.

DOI:10.2353/ajpath.2010.090615
PMID:20558573
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2893643/
Abstract

Atherosclerosis, a chronic vascular disease, is the underlying cause of over half the deaths in the United States each year. Variations in local vascular hemodynamics predispose select sites in the vasculature to atherosclerosis, and the atherosclerotic lesions, in turn alter the biomechanical functioning of the local microenvironment, the consequences of which are not well understood on a molecular level. Further progress in the field of atherosclerosis will require an understanding of the relationship between biomechanics, the tissue microenvironment, and the cellular and molecular response to these factors. This review summarizes this field, particularly within the context of the vascular smooth muscle cell.

摘要

动脉粥样硬化是一种慢性血管疾病,是导致美国每年半数以上死亡的根本原因。局部血管血液动力学的变化使血管的特定部位易发生动脉粥样硬化,而动脉粥样硬化病变又反过来改变局部微观环境的生物力学功能,但其在分子水平上的后果尚不清楚。在动脉粥样硬化领域取得进一步进展,需要了解生物力学、组织微环境以及细胞和分子对这些因素的反应之间的关系。本综述总结了这一领域,特别是在血管平滑肌细胞的背景下。

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本文引用的文献

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Unstable or High Risk Plaque: How Do We Approach It?不稳定或高危斑块:我们该如何应对?
Med J Armed Forces India. 2006 Jan;62(1):2-7. doi: 10.1016/S0377-1237(06)80141-3. Epub 2011 Jul 21.
2
Plaque volume compression ratio, a novel biomechanical index, is independently associated with ischemic cerebrovascular events.斑块体积压缩率是一种新型生物力学指标,与缺血性脑血管事件独立相关。
J Hypertens. 2009 Feb;27(2):348-56. doi: 10.1097/hjh.0b013e3283193e50.
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Ultrasonographic investigation of the mechanics of vulnerable atherosclerotic plaques: significance of the volume strain.易损动脉粥样硬化斑块力学特性的超声研究:体积应变的意义
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Regulation of the atheroma-enriched protein, SPRR3, in vascular smooth muscle cells through cyclic strain is dependent on integrin alpha1beta1/collagen interaction.通过周期性拉伸对富含动脉粥样硬化蛋白SPRR3在血管平滑肌细胞中的调控依赖于整合素α1β1/胶原蛋白相互作用。
Am J Pathol. 2008 Nov;173(5):1577-88. doi: 10.2353/ajpath.2008.080042. Epub 2008 Oct 2.
5
Angiotensin II upregulates LDL receptor-related protein (LRP1) expression in the vascular wall: a new pro-atherogenic mechanism of hypertension.血管紧张素II上调血管壁中低密度脂蛋白受体相关蛋白(LRP1)的表达:高血压一种新的促动脉粥样硬化机制。
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Over-expression of angiotensin II type 2 receptor (agtr2) reduces atherogenesis and modulates LOX-1, endothelial nitric oxide synthase and heme-oxygenase-1 expression.血管紧张素II 2型受体(agtr2)的过表达可减少动脉粥样硬化的发生,并调节凝集素样氧化低密度脂蛋白受体1(LOX-1)、内皮型一氧化氮合酶和血红素加氧酶-1的表达。
Atherosclerosis. 2008 Aug;199(2):288-94. doi: 10.1016/j.atherosclerosis.2007.11.006. Epub 2007 Dec 21.
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Calpain counteracts mechanosensitive apoptosis of vascular smooth muscle cells in vitro and in vivo.钙蛋白酶在体外和体内均可对抗血管平滑肌细胞的机械敏感性凋亡。
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Numerical analysis of pulsatile blood flow and vessel wall mechanics in different degrees of stenoses.不同程度狭窄情况下搏动性血流及血管壁力学的数值分析
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Frequency-dependent phenotype modulation of vascular smooth muscle cells under cyclic mechanical strain.循环机械应变下血管平滑肌细胞的频率依赖性表型调节
J Vasc Res. 2007;44(5):345-53. doi: 10.1159/000102278. Epub 2007 May 3.
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Mechano-pathobiology of atherogenesis: a review.动脉粥样硬化发生的机械病理生物学:综述
J Surg Res. 2007 Sep;142(1):202-17. doi: 10.1016/j.jss.2006.11.001. Epub 2007 Jul 5.