Shear stress and plaque development.
Although traditional cardiovascular risk factors 'prime the soil' for atherogenesis systemically, atherosclerosis primarily occurs in a site-specific manner with a predilection towards the inner wall of curvatures and outer wall of bifurcations with sparing of flow-dividers. Wall shear stress is a frictional force exerted parallel to the vessel wall that leads to alteration of the endothelial phenotype, endothelial cell signaling, gene and protein expression leading to a proinflammatory phenotype, reduced nitric oxide availability and disruption of the extracellular matrix, which in turn leads to plaque development. Clinical and experimental data are emerging that suggest the pathobiology associated with abnormal wall shear stress results in atherosclerotic plaque development and progression.
Dhawan
Saurabh S
SS
Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA 30322, USA.
Avati Nanjundappa
Ravi P
RP
Branch
Jonathan R
JR
Taylor
W Robert
WR
Quyyumi
Arshed A
AA
Jo
Hanjoong
H
McDaniel
Michael C
MC
Suo
Jin
J
Giddens
Don
D
Samady
Habib
H
D000818:Animals; D050197:Atherosclerosis / Q000209:etiology* / Q000503:physiopathology; D002339:Carotid Arteries / Q000503:physiopathology*; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D018384:Oxidative Stress; D012307:Risk Factors; D015398:Signal Transduction; D013314:Stress, Mechanical
D009569:Nitric Oxide
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