Serveur d'exploration sur la glutarédoxine

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Redox Signaling Mediated by Thioredoxin and Glutathione Systems in the Central Nervous System.

Identifieur interne : 000321 ( Main/Exploration ); précédent : 000320; suivant : 000322

Redox Signaling Mediated by Thioredoxin and Glutathione Systems in the Central Nervous System.

Auteurs : Xiaoyuan Ren [Suède] ; Lili Zou [Suède, République populaire de Chine] ; Xu Zhang [Suède] ; Vasco Branco [Portugal] ; Jun Wang [République populaire de Chine] ; Cristina Carvalho [Portugal] ; Arne Holmgren [Suède] ; Jun Lu [République populaire de Chine]

Source :

RBID : pubmed:28443683

Descripteurs français

English descriptors

Abstract

SIGNIFICANCE

The thioredoxin (Trx) and glutathione (GSH) systems play important roles in maintaining the redox balance in the brain, a tissue that is prone to oxidative stress due to its high-energy demand. These two disulfide reductase systems are active in various areas of the brain and are considered to be critical antioxidant systems in the central nervous system (CNS). Various neuronal disorders have been characterized to have imbalanced redox homeostasis. Recent Advances: In addition to their detrimental effects, recent studies have highlighted that reactive oxygen species/reactive nitrogen species (ROS/RNS) act as critical signaling molecules by modifying thiols in proteins. The Trx and GSH systems, which reversibly regulate thiol modifications, regulate redox signaling involved in various biological events in the CNS.

CRITICAL ISSUES

In this review, we focus on the following: (i) how ROS/RNS are produced and mediate signaling in CNS; (ii) how Trx and GSH systems regulate redox signaling by catalyzing reversible thiol modifications; (iii) how dysfunction of the Trx and GSH systems causes alterations of cellular redox signaling in human neuronal diseases; and (iv) the effects of certain small molecules that target thiol-based signaling pathways in the CNS.

FUTURE DIRECTIONS

Further study on the roles of thiol-dependent redox systems in the CNS will improve our understanding of the pathogenesis of many human neuronal disorders and also help to develop novel protective and therapeutic strategies against neuronal diseases. Antioxid. Redox Signal. 27, 989-1010.


DOI: 10.1089/ars.2016.6925
PubMed: 28443683
PubMed Central: PMC5649126


Affiliations:


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Le document en format XML

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<term>Reactive Nitrogen Species (metabolism)</term>
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<term>Glutathion (métabolisme)</term>
<term>Humains (MeSH)</term>
<term>Oxydoréduction (MeSH)</term>
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<b>SIGNIFICANCE</b>
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<p>The thioredoxin (Trx) and glutathione (GSH) systems play important roles in maintaining the redox balance in the brain, a tissue that is prone to oxidative stress due to its high-energy demand. These two disulfide reductase systems are active in various areas of the brain and are considered to be critical antioxidant systems in the central nervous system (CNS). Various neuronal disorders have been characterized to have imbalanced redox homeostasis. Recent Advances: In addition to their detrimental effects, recent studies have highlighted that reactive oxygen species/reactive nitrogen species (ROS/RNS) act as critical signaling molecules by modifying thiols in proteins. The Trx and GSH systems, which reversibly regulate thiol modifications, regulate redox signaling involved in various biological events in the CNS.</p>
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<p>
<b>CRITICAL ISSUES</b>
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<p>In this review, we focus on the following: (i) how ROS/RNS are produced and mediate signaling in CNS; (ii) how Trx and GSH systems regulate redox signaling by catalyzing reversible thiol modifications; (iii) how dysfunction of the Trx and GSH systems causes alterations of cellular redox signaling in human neuronal diseases; and (iv) the effects of certain small molecules that target thiol-based signaling pathways in the CNS.</p>
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<b>FUTURE DIRECTIONS</b>
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<p>Further study on the roles of thiol-dependent redox systems in the CNS will improve our understanding of the pathogenesis of many human neuronal disorders and also help to develop novel protective and therapeutic strategies against neuronal diseases. Antioxid. Redox Signal. 27, 989-1010.</p>
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