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10.1161/ATVBAHA.114.303422

http://scihub22266oqcxt.onion/10.1161/ATVBAHA.114.303422
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C4169328!4169328!24876354
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suck abstract from ncbi


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pmid24876354      Arterioscler+Thromb+Vasc+Biol 2014 ; 34 (10): 2191-8
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  • Shear stress-initiated signaling and its regulation of endothelial function #MMPMID24876354
  • Zhou J; Li YS; Chien S
  • Arterioscler Thromb Vasc Biol 2014[Oct]; 34 (10): 2191-8 PMID24876354show ga
  • Atherosclerosis develops preferentially at branches and curvatures of the arterial tree, where blood flow pattern is disturbed rather than being laminar, and wall shear stress has an irregular distribution without defined directions. The endothelium in the atherosusceptible regions, in comparison to that in atheroresistant regions, shows activation of pro-proliferative and pro-inflammatory gene expressions, reduced production of nitric oxide (NO), increased leukocyte adhesion and permeability, as well as other atheroprone phenotypes. Differences in gene expressions and cell phenotypes have been detected in endothelia residing in native atherosusceptible and atheroresistant regions of the arteries, or in arteries from animal models with artificial creation of disturbed flow. Similar results have also been shown in in vitro systems that apply controlled shear stresses with or without clear directions to cultured endothelial cells (ECs) in fluid-dynamically designed flow-loading devices. The available evidence indicates that the coordination of multiple signaling networks, rather than individual separate pathways, link the mechanical signals to specific genetic circuitries in orchestrating the mechanoresponsive networks to evoke comprehensive genetic and functional responses.
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