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Activation of Nrf2 in Endothelial Cells Protects Arteries From Exhibiting a Proinflammatory State
Author(s) -
Mustafa Zakkar,
Kim Van der Heiden,
Le Anh Luong,
Hera Chaudhury,
Chantal Simon,
Shahir Hamdulay,
Rob Krams,
Indika Edirisinghe,
Irfan Rahman,
Harald Carlsen,
Dorian O. Haskard,
Justin C. Mason,
Paul C. Evans
Publication year - 2009
Publication title -
arteriosclerosis, thrombosis, and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.109.193375
Subject(s) - proinflammatory cytokine , p38 mitogen activated protein kinases , microbiology and biotechnology , activator (genetics) , chemistry , endothelial activation , signal transduction , inflammation , transcription factor , regulator , biology , immunology , mapk/erk pathway , biochemistry , receptor , gene
Proinflammatory mediators influence atherosclerosis by inducing adhesion molecules (eg, VCAM-1) on endothelial cells (ECs) via signaling intermediaries including p38 MAP kinase. Regions of arteries exposed to high shear stress are protected from inflammation and atherosclerosis, whereas low-shear regions are susceptible. Here we investigated whether the transcription factor Nrf2 regulates EC activation in arteries.

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