Shear Stress and Atherosclerosis

被引:29
|
作者
Heo, Kyung-Sun [1 ]
Fujiwara, Keigi [1 ]
Abe, Jun-ichi [1 ]
机构
[1] Univ Rochester, Aab Cardiovasc Res Inst, Rochester, NY 14642 USA
关键词
chloride channel; ClC-1; myotonia congenital; skeletal muscle; OXIDE SYNTHASE EXPRESSION; SIGNAL-REGULATED KINASE-5; CELL-ADHESION MOLECULE-1; ENDOTHELIAL-CELLS; DISTURBED-FLOW; LESION FORMATION; PROTEASE; ACTIVATION; SUMOYLATION; MECHANOTRANSDUCTION;
D O I
10.14348/molcells.2014.0078
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Hemodynamic shear stress, the frictional force acting on vascular endothelial cells, is crucial for endothelial homeostasis under normal physiological conditions. When discussing blood flow effects on various forms of endothelial (dys) function, one considers two flow patterns: steady laminar flow and disturbed flow because endothelial cells respond differently to these flow types both in vivo and in vitro. Laminar flow which exerts steady laminar shear stress is atheroprotective while disturbed flow creates an atheroprone environment. Emerging evidence has provided new insights into the cellular mechanisms of flow-dependent regulation of vascular function that leads to cardiovascular events such as atherosclerosis, atherothrombosis, and myocardial infarction. In order to study effects of shear stress and different types of flow, various models have been used. In this review, we will summarize our current views on how disturbed flow-mediated signaling pathways are involved in the development of atherosclerosis.
引用
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页码:435 / 440
页数:6
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