Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance
Identifieur interne : 000118 ( Pmc/Corpus ); précédent : 000117; suivant : 000119Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance
Auteurs : S. Dalleau ; M. Baradat ; F. Guéraud ; L. HucSource :
- Cell Death and Differentiation [ 1350-9047 ] ; 2013.
Abstract
During the last three decades, 4-hydroxy-2-nonenal (HNE), a major
Url:
DOI: 10.1038/cdd.2013.138
PubMed: 24096871
PubMed Central: 3824598
Links to Exploration step
PMC:3824598Le document en format XML
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, 180 chemin de Tournefeuille, F-31027 Toulouse,<country>France</country>
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<author><name sortKey="Huc, L" sort="Huc, L" uniqKey="Huc L" first="L" last="Huc">L. Huc</name>
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<series><title level="j">Cell Death and Differentiation</title>
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<front><div type="abstract" xml:lang="en"><p>During the last three decades, 4-hydroxy-2-nonenal (HNE), a major <italic>α</italic>
,<italic>β-</italic>
unsaturated aldehyde product of n-6 fatty acid oxidation, has been shown to be involved in a great number of pathologies such as metabolic diseases, neurodegenerative diseases and cancers. These multiple pathologies can be explained by the fact that HNE is a potent modulator of numerous cell processes such as oxidative stress signaling, cell proliferation, transformation or cell death. The main objective of this review is to focus on the different aspects of HNE-induced cell death, with a particular emphasis on apoptosis. HNE is a special apoptotic inducer because of its abilities to form protein adducts and to propagate oxidative stress. It can stimulate intrinsic and extrinsic apoptotic pathways and interact with typical actors such as tumor protein 53, JNK, Fas or mitochondrial regulators. At the same time, due to its oxidant status, it can also induce some cellular defense mechanisms against oxidative stress, thus being involved in its own detoxification. These processes in turn limit the apoptotic potential of HNE. These dualities can imbalance cell fate, either toward cell death or toward survival, depending on the cell type, the metabolic state and the ability to detoxify.</p>
</div>
</front>
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<pmc article-type="review-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Cell Death Differ</journal-id>
<journal-id journal-id-type="iso-abbrev">Cell Death Differ</journal-id>
<journal-title-group><journal-title>Cell Death and Differentiation</journal-title>
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<issn pub-type="ppub">1350-9047</issn>
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<publisher><publisher-name>Nature Publishing Group</publisher-name>
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<article-meta><article-id pub-id-type="pmid">24096871</article-id>
<article-id pub-id-type="pmc">3824598</article-id>
<article-id pub-id-type="pii">cdd2013138</article-id>
<article-id pub-id-type="doi">10.1038/cdd.2013.138</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Review</subject>
</subj-group>
</article-categories>
<title-group><article-title>Cell death and diseases related to oxidative stress:4-hydroxynonenal (HNE) in the balance</article-title>
<alt-title alt-title-type="running">4-hydroxynonenal and mechanisms of cell death</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Dalleau</surname>
<given-names>S</given-names>
</name>
<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff2">2</xref>
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<contrib contrib-type="author"><name><surname>Baradat</surname>
<given-names>M</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff2">2</xref>
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<contrib contrib-type="author"><name><surname>Huc</surname>
<given-names>L</given-names>
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<xref ref-type="aff" rid="aff1">1</xref>
<xref ref-type="aff" rid="aff2">2</xref>
<xref ref-type="corresp" rid="caf1">*</xref>
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<aff id="aff1"><label>1</label>
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, 180 chemin de Tournefeuille, F-31027 Toulouse,<country>France</country>
</aff>
<aff id="aff2"><label>2</label>
<institution>Université de Toulouse III, INP, ENVT, UPS, TOXALIM</institution>
, F-31027 Toulouse,<country>France</country>
</aff>
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<author-notes><corresp id="caf1"><label>*</label>
<institution>INRA, TOXALIM (Research Centre in Food Toxicology)</institution>
, 180 chemin de Tournefeuille. F-31027 Toulouse, <country>France</country>
. Tel: +33 561285014; Fax: +33 561285244; E-mail: <email>Laurence.Huc@toulouse.inra.fr</email>
</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>12</month>
<year>2013</year>
</pub-date>
<pub-date pub-type="epub"><day>04</day>
<month>10</month>
<year>2013</year>
</pub-date>
<volume>20</volume>
<issue>12</issue>
<fpage>1615</fpage>
<lpage>1630</lpage>
<history><date date-type="received"><day>03</day>
<month>04</month>
<year>2013</year>
</date>
<date date-type="rev-recd"><day>22</day>
<month>07</month>
<year>2013</year>
</date>
<date date-type="accepted"><day>29</day>
<month>07</month>
<year>2013</year>
</date>
</history>
<permissions><copyright-statement>Copyright © 2013 Macmillan Publishers Limited</copyright-statement>
<copyright-year>2013</copyright-year>
<copyright-holder>Macmillan Publishers Limited</copyright-holder>
</permissions>
<abstract><p>During the last three decades, 4-hydroxy-2-nonenal (HNE), a major <italic>α</italic>
,<italic>β-</italic>
unsaturated aldehyde product of n-6 fatty acid oxidation, has been shown to be involved in a great number of pathologies such as metabolic diseases, neurodegenerative diseases and cancers. These multiple pathologies can be explained by the fact that HNE is a potent modulator of numerous cell processes such as oxidative stress signaling, cell proliferation, transformation or cell death. The main objective of this review is to focus on the different aspects of HNE-induced cell death, with a particular emphasis on apoptosis. HNE is a special apoptotic inducer because of its abilities to form protein adducts and to propagate oxidative stress. It can stimulate intrinsic and extrinsic apoptotic pathways and interact with typical actors such as tumor protein 53, JNK, Fas or mitochondrial regulators. At the same time, due to its oxidant status, it can also induce some cellular defense mechanisms against oxidative stress, thus being involved in its own detoxification. These processes in turn limit the apoptotic potential of HNE. These dualities can imbalance cell fate, either toward cell death or toward survival, depending on the cell type, the metabolic state and the ability to detoxify.</p>
</abstract>
<kwd-group><kwd>lipoperoxidation</kwd>
<kwd>apoptosis</kwd>
<kwd>detoxification</kwd>
<kwd>protein adduct</kwd>
<kwd>oxidative stress</kwd>
</kwd-group>
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</front>
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