Thioredoxin: a key regulator of cardiovascular homeostasis.
Identifieur interne : 000F03 ( Main/Exploration ); précédent : 000F02; suivant : 000F04Thioredoxin: a key regulator of cardiovascular homeostasis.
Auteurs : Hideyuki Yamawaki [États-Unis] ; Judith Haendeler ; Bradford C. BerkSource :
- Circulation research [ 1524-4571 ] ; 2003.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Antioxydants (métabolisme), Glutarédoxines (MeSH), Homéostasie (physiologie), Humains (MeSH), MAP Kinase Kinase Kinase 5 (MeSH), MAP Kinase Kinase Kinases (métabolisme), Oxidoreductases (MeSH), Oxydoréduction (MeSH), Protéines (métabolisme), Protéines de transport (métabolisme), Stress oxydatif (physiologie), Système cardiovasculaire (métabolisme), Thiorédoxines (métabolisme), Transduction du signal (physiologie).
- MESH :
English descriptors
- KwdEn :
- Animals (MeSH), Antioxidants (metabolism), Cardiovascular System (metabolism), Carrier Proteins (metabolism), Glutaredoxins (MeSH), Homeostasis (physiology), Humans (MeSH), MAP Kinase Kinase Kinase 5 (MeSH), MAP Kinase Kinase Kinases (metabolism), Oxidation-Reduction (MeSH), Oxidative Stress (physiology), Oxidoreductases (MeSH), Proteins (metabolism), Signal Transduction (physiology), Thioredoxins (metabolism).
- MESH :
- chemical , metabolism : Antioxidants, Carrier Proteins, MAP Kinase Kinase Kinases, Proteins, Thioredoxins.
- metabolism : Cardiovascular System.
- physiology : Homeostasis, Oxidative Stress, Signal Transduction.
- Animals, Glutaredoxins, Humans, MAP Kinase Kinase Kinase 5, Oxidation-Reduction, Oxidoreductases.
Abstract
The thioredoxin (TRX) system (TRX, TRX reductase, and NADPH) is a ubiquitous thiol oxidoreductase system that regulates cellular reduction/oxidation (redox) status. The oxidation mechanism for disease pathogenesis states that an imbalance in cell redox state alters function of multiple cell pathways. In this study, we review the essential role for TRX to limit oxidative stress directly via antioxidant effects and indirectly by protein-protein interaction with key signaling molecules, such as apoptosis signal-regulating kinase 1. We propose that TRX and its endogenous regulators are important future targets to develop clinical therapies for cardiovascular disorders associated with oxidative stress.
DOI: 10.1161/01.RES.0000102869.39150.23
PubMed: 14645133
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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The oxidation mechanism for disease pathogenesis states that an imbalance in cell redox state alters function of multiple cell pathways. In this study, we review the essential role for TRX to limit oxidative stress directly via antioxidant effects and indirectly by protein-protein interaction with key signaling molecules, such as apoptosis signal-regulating kinase 1. 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The oxidation mechanism for disease pathogenesis states that an imbalance in cell redox state alters function of multiple cell pathways. In this study, we review the essential role for TRX to limit oxidative stress directly via antioxidant effects and indirectly by protein-protein interaction with key signaling molecules, such as apoptosis signal-regulating kinase 1. 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Berk</name><name sortKey="Haendeler, Judith" sort="Haendeler, Judith" uniqKey="Haendeler J" first="Judith" last="Haendeler">Judith Haendeler</name></noCountry><country name="États-Unis"><region name="État de New York"><name sortKey="Yamawaki, Hideyuki" sort="Yamawaki, Hideyuki" uniqKey="Yamawaki H" first="Hideyuki" last="Yamawaki">Hideyuki Yamawaki</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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