Journal
JOURNAL OF THE ROYAL SOCIETY INTERFACE
Volume 8, Issue 63, Pages 1379-1385Publisher
ROYAL SOC
DOI: 10.1098/rsif.2011.0177
Keywords
mechanical transduction; laminar shear stress; circumferential stretch; endothelial cells; smooth muscle cells; oxidative stress
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Funding
- National Heart, Lung, and Blood Institute [HL-084 529, HL-055 554-12]
- National Institute of Health [HL084 529, HL055 554-11]
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Blood vessels are under constant mechanical loading from blood pressure and flow which cause internal stresses (endothelial shear stress and circumferential wall stress, respectively). The mechanical forces not only cause morphological changes of endothelium and blood vessel wall, but also trigger biochemical and biological events. There is considerable evidence that physiologic stresses and strains (stretch) exert vasoprotective roles via nitric oxide and provide a homeostatic oxidative balance. A perturbation of tissue stresses and strains can disturb biochemical homeostasis and lead to vascular remodelling and possible dysfunction (e. g. altered vasorelaxation, tone, stiffness, etc.). These distinct biological endpoints are caused by some common biochemical pathways. The focus of this brief review is to point out some possible commonalities in the molecular pathways in response to endothelial shear stress and circumferential wall stretch.
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