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血管剪切应力与炎症基因的激活

Vascular shear stress and activation of inflammatory genes.

作者信息

World Cameron J, Garin Gwenaele, Berk Bradford

机构信息

Cardiovascular Research Institute, University of Rochester, 601 Elmwood Avenue, Rochester, NY 14642, USA.

出版信息

Curr Atheroscler Rep. 2006 May;8(3):240-4. doi: 10.1007/s11883-006-0079-8.

Abstract

Atherosclerotic lesions form preferentially at distinct sites in the arterial tree, especially at or near branch points, bifurcations, and curvatures where there is disturbed or oscillatory blood flow. In contrast, straight regions of the vasculature exhibit uniform laminar shear stress, which is atheroprotective. The ability of laminar flow to exert an anti-inflammatory effect on the endothelial cell lining of the blood vessel is revealed by preventing monocyte adhesion, proliferation, and apoptosis. Changes in endothelial cell gene expression in response to laminar shear stress reflect these changes in cell physiology with the demonstration that physiologic flow inhibits the expression of inflammatory genes. Thus, shear stress is critically important in regulating vascular physiology and pathobiology of the vessel wall via the modulation of endothelial cell gene expression.

摘要

动脉粥样硬化病变优先在动脉系统的特定部位形成,尤其是在分支点、分叉处和曲率处或其附近,这些部位存在紊乱或振荡的血流。相比之下,血管的直管区域表现出均匀的层流切应力,这具有抗动脉粥样硬化作用。层流通过阻止单核细胞黏附、增殖和凋亡,显示出对血管内皮细胞衬里具有抗炎作用。响应层流切应力时内皮细胞基因表达的变化反映了细胞生理学的这些变化,表明生理血流抑制炎症基因的表达。因此,切应力通过调节内皮细胞基因表达在调节血管生理和血管壁病理生物学方面至关重要。

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