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The Redox Code

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Antioxidants & Redox Signaling

Mary Ann Liebert, Inc.

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      Significance: The redox code is a set of principles that defines the positioning of the nicotinamide adenine dinucleotide (NAD, NADP) and thiol/disulfide and other redox systems as well as the thiol redox proteome in space and time in biological systems. The code is richly elaborated in an oxygen-dependent life, where activation/deactivation cycles involving O 2 and H 2O 2 contribute to spatiotemporal organization for differentiation, development, and adaptation to the environment. Disruption of this organizational structure during oxidative stress represents a fundamental mechanism in system failure and disease. Recent Advances: Methodology in assessing components of the redox code under physiological conditions has progressed, permitting insight into spatiotemporal organization and allowing for identification of redox partners in redox proteomics and redox metabolomics. Critical Issues: Complexity of redox networks and redox regulation is being revealed step by step, yet much still needs to be learned. Future Directions: Detailed knowledge of the molecular patterns generated from the principles of the redox code under defined physiological or pathological conditions in cells and organs will contribute to understanding the redox component in health and disease. Ultimately, there will be a scientific basis to a modern redox medicine. Antioxid. Redox Signal. 23, 734–746.

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      Most cited references 121

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      Aging is characterized by a progressive loss of physiological integrity, leading to impaired function and increased vulnerability to death. This deterioration is the primary risk factor for major human pathologies, including cancer, diabetes, cardiovascular disorders, and neurodegenerative diseases. Aging research has experienced an unprecedented advance over recent years, particularly with the discovery that the rate of aging is controlled, at least to some extent, by genetic pathways and biochemical processes conserved in evolution. This Review enumerates nine tentative hallmarks that represent common denominators of aging in different organisms, with special emphasis on mammalian aging. These hallmarks are: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. A major challenge is to dissect the interconnectedness between the candidate hallmarks and their relative contributions to aging, with the final goal of identifying pharmaceutical targets to improve human health during aging, with minimal side effects. Copyright © 2013 Elsevier Inc. All rights reserved.
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        A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis.

        Adaptive thermogenesis is an important component of energy homeostasis and a metabolic defense against obesity. We have cloned a novel transcriptional coactivator of nuclear receptors, termed PGC-1, from a brown fat cDNA library. PGC-1 mRNA expression is dramatically elevated upon cold exposure of mice in both brown fat and skeletal muscle, key thermogenic tissues. PGC-1 greatly increases the transcriptional activity of PPARgamma and the thyroid hormone receptor on the uncoupling protein (UCP-1) promoter. Ectopic expression of PGC-1 in white adipose cells activates expression of UCP-1 and key mitochondrial enzymes of the respiratory chain, and increases the cellular content of mitochondrial DNA. These results indicate that PGC-1 plays a key role in linking nuclear receptors to the transcriptional program of adaptive thermogenesis.
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          ROS as signalling molecules: mechanisms that generate specificity in ROS homeostasis.

          Reactive oxygen species (ROS) have been shown to be toxic but also function as signalling molecules. This biological paradox underlies mechanisms that are important for the integrity and fitness of living organisms and their ageing. The pathways that regulate ROS homeostasis are crucial for mitigating the toxicity of ROS and provide strong evidence about specificity in ROS signalling. By taking advantage of the chemistry of ROS, highly specific mechanisms have evolved that form the basis of oxidant scavenging and ROS signalling systems.

            Author and article information

            [ 1 ]Department of Medicine, Emory University , Atlanta, Georgia.
            [ 2 ]Institute for Biochemistry and Molecular Biology I, Heinrich Heine University Düsseldorf , Düsseldorf, Germany.
            [ 3 ]Leibniz Research Institute for Environmental Medicine, Heinrich Heine University Düsseldorf , Düsseldorf, Germany.
            Author notes
            Address correspondence to: Prof. Helmut Sies, Institute for Biochemistry and Molecular Biology I, Heinrich Heine University Düsseldorf Building 22.03, Universitätsstrasse 1, Düsseldorf D-40225, Germany

            E-mail: sies@
            Antioxid Redox Signal
            Antioxid. Redox Signal
            Antioxidants & Redox Signaling
            Mary Ann Liebert, Inc. (140 Huguenot Street, 3rd FloorNew Rochelle, NY 10801USA )
            20 September 2015
            20 September 2015
            : 23
            : 9
            : 734-746
            25891126 4580308 10.1089/ars.2015.6247 10.1089/ars.2015.6247
            © Dean P. Jones and Helmut Sies 2015; Published by Mary Ann Liebert, Inc.

            This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License ( which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.

            Figures: 5, Tables: 1, References: 127, Pages: 13
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