共 65 条
Redox-dependent transcriptional regulation
被引:340
作者:

Liu, HJ
论文数: 0 引用数: 0
h-index: 0
机构:
NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA

Colavitti, R
论文数: 0 引用数: 0
h-index: 0
机构:
NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA

Rovira, II
论文数: 0 引用数: 0
h-index: 0
机构:
NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA

Finkel, T
论文数: 0 引用数: 0
h-index: 0
机构:
NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA
机构:
[1] NIH, Cardiol Branch, NHLBI, Bethesda, MD 20892 USA
关键词:
Yap1;
ref;
Nrf2;
atherosclerosis;
oxidative stress;
D O I:
10.1161/01.RES.0000188210.72062.10
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Reactive oxygen species contribute to the pathogenesis of a number of disparate disorders including tissue inflammation, heart failure, hypertension, and atherosclerosis. In response to oxidative stress, cells activate expression of a number of genes, including those required for the detoxification of reactive molecules as well as for the repair and maintenance of cellular homeostasis. In many cases, these induced genes are regulated by transcription factors whose structure, subcellular localization, or affinity for DNA is directly or indirectly regulated by the level of oxidative stress. This review summarizes the recent progress on how cellular redox status can regulate transcription-factor activity and the implications of this regulation for cardiovascular disease.
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收藏
页码:967 / 974
页数:8
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