GlutaredoxinV1, Main, Exploration, bibRecord, 000E37

Thioredoxin regulation of ischemic preconditioning.

Identifieur interne : 000E37 ( Main/Exploration ); précédent : 000E36; suivant : 000E38

Thioredoxin regulation of ischemic preconditioning.

Auteurs : Dipak K. Das [États-Unis]

Source :

Antioxidants & redox signaling [ 1523-0864 ] ; 2004.

RBID : pubmed:15025942

Descripteurs français

KwdFr :
- Animaux (MeSH), Glutarédoxines (MeSH), Ischémie myocardique (anatomopathologie), Ischémie myocardique (métabolisme), Lésion de reperfusion myocardique (anatomopathologie), Lésion de reperfusion myocardique (métabolisme), Oxidoreductases (métabolisme), Oxydoréduction (MeSH), Préconditionnement ischémique myocardique (MeSH), Thiorédoxines (génétique), Thiorédoxines (métabolisme), Transduction du signal (physiologie).
MESH :
- anatomopathologie : Ischémie myocardique, Lésion de reperfusion myocardique.
- génétique : Thiorédoxines.
- métabolisme : Ischémie myocardique, Lésion de reperfusion myocardique, Oxidoreductases, Thiorédoxines.
- physiologie : Transduction du signal.
- Animaux, Glutarédoxines, Oxydoréduction, Préconditionnement ischémique myocardique.

English descriptors

KwdEn :
- Animals (MeSH), Glutaredoxins (MeSH), Ischemic Preconditioning, Myocardial (MeSH), Myocardial Ischemia (metabolism), Myocardial Ischemia (pathology), Myocardial Reperfusion Injury (metabolism), Myocardial Reperfusion Injury (pathology), Oxidation-Reduction (MeSH), Oxidoreductases (metabolism), Signal Transduction (physiology), Thioredoxins (genetics), Thioredoxins (metabolism).
MESH :
- chemical , genetics : Thioredoxins.
- chemical , metabolism : Oxidoreductases, Thioredoxins.
- chemical : Glutaredoxins.
- metabolism : Myocardial Ischemia, Myocardial Reperfusion Injury.
- pathology : Myocardial Ischemia, Myocardial Reperfusion Injury.
- physiology : Signal Transduction.
- Animals, Ischemic Preconditioning, Myocardial, Oxidation-Reduction.

Abstract

Thioredoxins are a class of small redox-regulating proteins that appear to play a crucial role in many oxidative stress-inducible degenerative diseases. A recent study demonstrated a reduction of thioredoxin-1 (Trx1) protein in the ischemic reperfused myocardium. When the same heart was adapted to ischemic stress by preconditioning with repeated cyclic episodes of small duration of ischemia and reperfusion, there was an increased induction of Trx1 expression. Inhibition of Trx1 expression resulted in reduced postischemic ventricular recovery and increased myocardial infarct size in the preconditioned heart. Corroborating these findings, transgenic mouse hearts overexpressing Trx1 were resistant to ischemic reperfusion injury as compared with the hearts from wild-type mice. Thus, it appears that thioredoxin plays a crucial role in cardioprotection induced by preconditioning.

DOI: 10.1089/152308604322899477
PubMed: 15025942

Affiliations:

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Le document en format XML

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<author><name sortKey="Das, Dipak K" sort="Das, Dipak K" uniqKey="Das D" first="Dipak K" last="Das">Dipak K. Das</name>
<affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, CT, USA. DDAS@NEURON.UCHC.EDU</nlm:affiliation>
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<term>Glutaredoxins (MeSH)</term>
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<term>Myocardial Ischemia (metabolism)</term>
<term>Myocardial Ischemia (pathology)</term>
<term>Myocardial Reperfusion Injury (metabolism)</term>
<term>Myocardial Reperfusion Injury (pathology)</term>
<term>Oxidation-Reduction (MeSH)</term>
<term>Oxidoreductases (metabolism)</term>
<term>Signal Transduction (physiology)</term>
<term>Thioredoxins (genetics)</term>
<term>Thioredoxins (metabolism)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Glutarédoxines (MeSH)</term>
<term>Ischémie myocardique (anatomopathologie)</term>
<term>Ischémie myocardique (métabolisme)</term>
<term>Lésion de reperfusion myocardique (anatomopathologie)</term>
<term>Lésion de reperfusion myocardique (métabolisme)</term>
<term>Oxidoreductases (métabolisme)</term>
<term>Oxydoréduction (MeSH)</term>
<term>Préconditionnement ischémique myocardique (MeSH)</term>
<term>Thiorédoxines (génétique)</term>
<term>Thiorédoxines (métabolisme)</term>
<term>Transduction du signal (physiologie)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Thioredoxins</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Oxidoreductases</term>
<term>Thioredoxins</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Glutaredoxins</term>
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<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Ischémie myocardique</term>
<term>Lésion de reperfusion myocardique</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Thiorédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Myocardial Ischemia</term>
<term>Myocardial Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Ischémie myocardique</term>
<term>Lésion de reperfusion myocardique</term>
<term>Oxidoreductases</term>
<term>Thiorédoxines</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Myocardial Ischemia</term>
<term>Myocardial Reperfusion Injury</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Transduction du signal</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Signal Transduction</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Ischemic Preconditioning, Myocardial</term>
<term>Oxidation-Reduction</term>
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<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Glutarédoxines</term>
<term>Oxydoréduction</term>
<term>Préconditionnement ischémique myocardique</term>
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<front><div type="abstract" xml:lang="en">Thioredoxins are a class of small redox-regulating proteins that appear to play a crucial role in many oxidative stress-inducible degenerative diseases. A recent study demonstrated a reduction of thioredoxin-1 (Trx1) protein in the ischemic reperfused myocardium. When the same heart was adapted to ischemic stress by preconditioning with repeated cyclic episodes of small duration of ischemia and reperfusion, there was an increased induction of Trx1 expression. Inhibition of Trx1 expression resulted in reduced postischemic ventricular recovery and increased myocardial infarct size in the preconditioned heart. Corroborating these findings, transgenic mouse hearts overexpressing Trx1 were resistant to ischemic reperfusion injury as compared with the hearts from wild-type mice. Thus, it appears that thioredoxin plays a crucial role in cardioprotection induced by preconditioning.</div>
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<Title>Antioxidants & redox signaling</Title>
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<Abstract><AbstractText>Thioredoxins are a class of small redox-regulating proteins that appear to play a crucial role in many oxidative stress-inducible degenerative diseases. A recent study demonstrated a reduction of thioredoxin-1 (Trx1) protein in the ischemic reperfused myocardium. When the same heart was adapted to ischemic stress by preconditioning with repeated cyclic episodes of small duration of ischemia and reperfusion, there was an increased induction of Trx1 expression. Inhibition of Trx1 expression resulted in reduced postischemic ventricular recovery and increased myocardial infarct size in the preconditioned heart. Corroborating these findings, transgenic mouse hearts overexpressing Trx1 were resistant to ischemic reperfusion injury as compared with the hearts from wild-type mice. Thus, it appears that thioredoxin plays a crucial role in cardioprotection induced by preconditioning.</AbstractText>
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Thioredoxin regulation of ischemic preconditioning.

Thioredoxin regulation of ischemic preconditioning.

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

Pour mettre un lien sur cette page dans le réseau Wicri

Pour générer des pages wiki