Circulation Research. 2005;97:967-974
doi: 10.1161/01.RES.0000188210.72062.10
doi: 10.1161/01.RES.0000188210.72062.10
© 2005 American Heart Association, Inc.
Review |
Redox-Dependent Transcriptional Regulation
From the Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.
Correspondence to Toren Finkel, MD, PhD, Chief, Cardiology Branch, National Institutes of Health, Bldg 10 CRC 5-3330, 10 Center Dr, Bethesda, MD 20892. E-mail finkelt{at}nih.gov
Editor: This Review is part of a thematic series on New Paradigms of Transcriptional Control of Myocardial and Vascular Growth, which includes the following articles:
Redox-Dependent Transcriptional Regulation
Excitation-Transcription Coupling
Histone-Modulation as a Regulator of Growth
Gordon F. Tomaselli
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.
Key Words: Yap1 • ref-1 • Nrf2 • atherosclerosis • oxidative stress
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