Effect of shear stress on vascular inflammation and plaque development.
OBJECTIVE
This review describes evidence that shear stress acts through modulation of inflammation and by that process affects atherogenesis and plaque composition.


RESULTS
In low shear stress regions antiatherogenic transcription factors are downregulated and pro-atherogenic transcription factors are upregulated. Consequently, inflammatory cells may home low shear stress regions more easily to the plaques because of increased expression of adhesion factors, a decreased rolling speed and an increased expression of chemokines, thereby changing the composition of the plaques into a more vulnerable phenotype. In contrast, in advanced plaque development vascular lumen decreases and shear stress increases, especially upstream of the plaques. The predominant upstream location of lipids induces a prevalent upstream location of inflammatory cells leading to localized plaque rupture.


CONCLUSIONS
Shear stress has been shown to play a role in plaque induction, plaque progression and plaque rupture. The mechanism for plaque induction seems to differ from the role of shear stress for plaque rupture, whereby the former mechanism is induced by low shear stress and the latter by high shear stress.
Helderman
Frank
F
Department of Physics, Free University of Amsterdam, The Netherlands.
Segers
Dolf
D
de Crom
Rini
R
Hierck
Berend P
BP
Poelmann
Rob E
RE
Evans
Paul C
PC
Krams
Rob
R
D000818:Animals; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D001808:Blood Vessels / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D050356:Lipid Metabolism; D008954:Models, Biological; D013314:Stress, Mechanical; D014657:Vasculitis / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*
D018836:Inflammation Mediators