Role of Nrf2 in the pathogenesis of atherosclerosis

被引:111
|
作者
Mimura, Junsei [1 ]
Itoh, Ken [1 ]
机构
[1] Hirosaki Univ, Dept Stress Response Sci, Grad Sch Med, Hirosaki, Aomori 0368562, Japan
关键词
Atherosclerosis; Nrf2; Oxidative stress; Inflammation; Oxidized LDL; Lipid metabolism; Endothelial cell; Smooth muscle cell; Macrophage; CD36; LOW-DENSITY-LIPOPROTEIN; SMOOTH-MUSCLE-CELL; TRANSCRIPTION FACTOR NRF2; MACROPHAGE SCAVENGER RECEPTORS; ANTIOXIDANT RESPONSE ELEMENT; E-DEFICIENT MICE; OXIDATIVE STRESS; HEME OXYGENASE-1; GLUTATHIONE SYNTHESIS; GENE-EXPRESSION;
D O I
10.1016/j.freeradbiomed.2015.06.019
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Atherosclerosis is a chronic inflammatory disease of the vascular arterial walls. A number of studies have revealed the biological and genetic bases of atherosclerosis, and over 100 genes influence atherosclerosis development. Nrf2 plays an important role in oxidative stress response and drug metabolism, but the Nrf2 signaling pathway is closely associated with atherosclerosis development. During atherosclerosis progression, Nrf2 signaling modulates many physiological and pathophysiological processes, such as lipid homeostasis regulation, foam cell formation, macrophage polarization, redox regulation and inflammation. Interestingly, Nrf2 exhibits both pro- and anti-atherogenic effects in experimental animal models. These observations make the Nrf2 pathway a promising target to prevent atherosclerosis. (C) 2015 Published by Elsevier Inc.
引用
收藏
页码:221 / 232
页数:12
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