[SIRT1/PGC-1: a neuroprotective axis?].
Identifieur interne : 002586 ( Main/Exploration ); précédent : 002585; suivant : 002587[SIRT1/PGC-1: a neuroprotective axis?].
Auteurs : Soumya Rasouri [France] ; Marie Lagouge ; Johan AuwerxSource :
- Medecine sciences : M/S [ 0767-0974 ] ; 2007.
English descriptors
- KwdEn :
- Acetylation, Amyloid beta-Peptides (metabolism), Animals, Cells, Cultured (drug effects), Humans, Mice, Mice, Knockout, Mice, Transgenic, Mitochondria (physiology), Neurodegenerative Diseases (metabolism), Neurodegenerative Diseases (physiopathology), Neurodegenerative Diseases (prevention & control), Neurons (drug effects), Neurons (metabolism), Neurons (pathology), Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Protein Processing, Post-Translational (drug effects), Reactive Oxygen Species, Sirtuin 1, Sirtuins (genetics), Sirtuins (physiology), Stilbenes (pharmacology), Stilbenes (therapeutic use), Transcription Factors (deficiency), Transcription Factors (genetics), Transcription Factors (physiology), Transcriptional Activation.
- MESH :
- chemical , deficiency : Transcription Factors.
- chemical , genetics : Sirtuins, Transcription Factors.
- chemical , metabolism : Amyloid beta-Peptides.
- drug effects : Cells, Cultured, Neurons, Protein Processing, Post-Translational.
- metabolism : Neurodegenerative Diseases, Neurons.
- pathology : Neurons.
- chemical , pharmacology : Neuroprotective Agents, Stilbenes.
- physiology : Mitochondria, Sirtuins, Transcription Factors.
- physiopathology : Neurodegenerative Diseases.
- prevention & control : Neurodegenerative Diseases.
- chemical , therapeutic use : Neuroprotective Agents, Stilbenes.
- Acetylation, Animals, Humans, Mice, Mice, Knockout, Mice, Transgenic, Reactive Oxygen Species, Sirtuin 1, Transcriptional Activation.
Abstract
Neurodegenerative diseases are more and more prevalent in our aging societies. A rapid overview of the etiology of many neurodegenerative diseases like Alzheimer, Parkinson, Huntington disease and amyotrophic lateral sclerosis suggests a tight link with mitochondrial dysfunction. Since it has been recently demonstrated that activation of the SIRT1/PGC-1 pathway, in a metabolic context promotes mitochondrial function, we performed a detailed literature review on the implication of this pathway in neurodegeneration. Interestingly, transgenic mice with impaired PGC-1 expression have neurodegenerative lesions and show behavioural abnormalities. As evidenced from independent investigations, enhanced SIRT1 activity has been demonstrated to protect against axonal degeneration and to decrease the accumulation of amyloid beta peptides, the hallmark of Alzheimer disease, in cultured murine embryonic neurons. In addition, several studies suggest that resveratrol, a specific activator of SIRT1, could have protective effects in animal models of neurodegenerative diseases. Taken together, these results strongly suggest that the modulation of the SIRT1/PGC-1 pathway, which has not been well documented in the central nervous system, could become the cornerstone for new therapeutical approaches to combat neurodegeneration.
Url:
DOI: 10.1051/medsci/20072310840
PubMed: 17937892
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 000D53
- to stream PubMed, to step Curation: 000D13
- to stream PubMed, to step Checkpoint: 000D13
- to stream Ncbi, to step Merge: 000779
- to stream Ncbi, to step Curation: 000779
- to stream Ncbi, to step Checkpoint: 000779
- to stream Main, to step Merge: 002828
- to stream Hal, to step Corpus: 000C82
- to stream Hal, to step Curation: 000C82
- to stream Hal, to step Checkpoint: 000954
- to stream Main, to step Merge: 002799
- to stream Main, to step Curation: 002586
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">[SIRT1/PGC-1: a neuroprotective axis?].</title>
<author><name sortKey="Rasouri, Soumya" sort="Rasouri, Soumya" uniqKey="Rasouri S" first="Soumya" last="Rasouri">Soumya Rasouri</name>
<affiliation wicri:level="3"><nlm:affiliation>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/Inserm/ULP, 1, rue Laurent Fries, 67404 Illkirch, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/Inserm/ULP, 1, rue Laurent Fries, 67404 Illkirch</wicri:regionArea>
<placeName><region type="region" nuts="2">Grand Est</region>
<region type="old region" nuts="2">Alsace (région administrative)</region>
<settlement type="city">Illkirch</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lagouge, Marie" sort="Lagouge, Marie" uniqKey="Lagouge M" first="Marie" last="Lagouge">Marie Lagouge</name>
</author>
<author><name sortKey="Auwerx, Johan" sort="Auwerx, Johan" uniqKey="Auwerx J" first="Johan" last="Auwerx">Johan Auwerx</name>
</author>
</titleStmt>
<publicationStmt><idno type="wicri:source">PubMed</idno>
<date when="2007">2007</date>
<idno type="RBID">pubmed:17937892</idno>
<idno type="pmid">17937892</idno>
<idno type="doi">10.1051/medsci/20072310840</idno>
<idno type="wicri:Area/PubMed/Corpus">000D53</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D53</idno>
<idno type="wicri:Area/PubMed/Curation">000D13</idno>
<idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000D13</idno>
<idno type="wicri:Area/PubMed/Checkpoint">000D13</idno>
<idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000D13</idno>
<idno type="wicri:Area/Ncbi/Merge">000779</idno>
<idno type="wicri:Area/Ncbi/Curation">000779</idno>
<idno type="wicri:Area/Ncbi/Checkpoint">000779</idno>
<idno type="wicri:doubleKey">0767-0974:2007:Rasouri S:sirt:pgc:a</idno>
<idno type="wicri:Area/Main/Merge">002828</idno>
<idno type="wicri:source">HAL</idno>
<idno type="RBID">Hal:hal-00188845</idno>
<idno type="url">https://hal.archives-ouvertes.fr/hal-00188845</idno>
<idno type="wicri:Area/Hal/Corpus">000C82</idno>
<idno type="wicri:Area/Hal/Curation">000C82</idno>
<idno type="wicri:Area/Hal/Checkpoint">000954</idno>
<idno type="wicri:explorRef" wicri:stream="Hal" wicri:step="Checkpoint">000954</idno>
<idno type="wicri:doubleKey">0767-0974:2007:Rasouri S:sirt:pgc:a</idno>
<idno type="wicri:Area/Main/Merge">002799</idno>
<idno type="wicri:Area/Main/Curation">002586</idno>
<idno type="wicri:Area/Main/Exploration">002586</idno>
</publicationStmt>
<sourceDesc><biblStruct><analytic><title xml:lang="en">[SIRT1/PGC-1: a neuroprotective axis?].</title>
<author><name sortKey="Rasouri, Soumya" sort="Rasouri, Soumya" uniqKey="Rasouri S" first="Soumya" last="Rasouri">Soumya Rasouri</name>
<affiliation wicri:level="3"><nlm:affiliation>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/Inserm/ULP, 1, rue Laurent Fries, 67404 Illkirch, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/Inserm/ULP, 1, rue Laurent Fries, 67404 Illkirch</wicri:regionArea>
<placeName><region type="region" nuts="2">Grand Est</region>
<region type="old region" nuts="2">Alsace (région administrative)</region>
<settlement type="city">Illkirch</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Lagouge, Marie" sort="Lagouge, Marie" uniqKey="Lagouge M" first="Marie" last="Lagouge">Marie Lagouge</name>
</author>
<author><name sortKey="Auwerx, Johan" sort="Auwerx, Johan" uniqKey="Auwerx J" first="Johan" last="Auwerx">Johan Auwerx</name>
</author>
</analytic>
<series><title level="j">Medecine sciences : M/S</title>
<idno type="ISSN">0767-0974</idno>
<imprint><date when="2007" type="published">2007</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Acetylation</term>
<term>Amyloid beta-Peptides (metabolism)</term>
<term>Animals</term>
<term>Cells, Cultured (drug effects)</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Mice, Transgenic</term>
<term>Mitochondria (physiology)</term>
<term>Neurodegenerative Diseases (metabolism)</term>
<term>Neurodegenerative Diseases (physiopathology)</term>
<term>Neurodegenerative Diseases (prevention & control)</term>
<term>Neurons (drug effects)</term>
<term>Neurons (metabolism)</term>
<term>Neurons (pathology)</term>
<term>Neuroprotective Agents (pharmacology)</term>
<term>Neuroprotective Agents (therapeutic use)</term>
<term>Protein Processing, Post-Translational (drug effects)</term>
<term>Reactive Oxygen Species</term>
<term>Sirtuin 1</term>
<term>Sirtuins (genetics)</term>
<term>Sirtuins (physiology)</term>
<term>Stilbenes (pharmacology)</term>
<term>Stilbenes (therapeutic use)</term>
<term>Transcription Factors (deficiency)</term>
<term>Transcription Factors (genetics)</term>
<term>Transcription Factors (physiology)</term>
<term>Transcriptional Activation</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Sirtuins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Amyloid beta-Peptides</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cells, Cultured</term>
<term>Neurons</term>
<term>Protein Processing, Post-Translational</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurodegenerative Diseases</term>
<term>Neurons</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Neurons</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective Agents</term>
<term>Stilbenes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Mitochondria</term>
<term>Sirtuins</term>
<term>Transcription Factors</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Neurodegenerative Diseases</term>
</keywords>
<keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Neurodegenerative Diseases</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term>
<term>Stilbenes</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Acetylation</term>
<term>Animals</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Knockout</term>
<term>Mice, Transgenic</term>
<term>Reactive Oxygen Species</term>
<term>Sirtuin 1</term>
<term>Transcriptional Activation</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Neurodegenerative diseases are more and more prevalent in our aging societies. A rapid overview of the etiology of many neurodegenerative diseases like Alzheimer, Parkinson, Huntington disease and amyotrophic lateral sclerosis suggests a tight link with mitochondrial dysfunction. Since it has been recently demonstrated that activation of the SIRT1/PGC-1 pathway, in a metabolic context promotes mitochondrial function, we performed a detailed literature review on the implication of this pathway in neurodegeneration. Interestingly, transgenic mice with impaired PGC-1 expression have neurodegenerative lesions and show behavioural abnormalities. As evidenced from independent investigations, enhanced SIRT1 activity has been demonstrated to protect against axonal degeneration and to decrease the accumulation of amyloid beta peptides, the hallmark of Alzheimer disease, in cultured murine embryonic neurons. In addition, several studies suggest that resveratrol, a specific activator of SIRT1, could have protective effects in animal models of neurodegenerative diseases. Taken together, these results strongly suggest that the modulation of the SIRT1/PGC-1 pathway, which has not been well documented in the central nervous system, could become the cornerstone for new therapeutical approaches to combat neurodegeneration.</div>
</front>
</TEI>
<affiliations><list><country><li>France</li>
</country>
<region><li>Alsace (région administrative)</li>
<li>Grand Est</li>
</region>
<settlement><li>Illkirch</li>
</settlement>
</list>
<tree><noCountry><name sortKey="Auwerx, Johan" sort="Auwerx, Johan" uniqKey="Auwerx J" first="Johan" last="Auwerx">Johan Auwerx</name>
<name sortKey="Lagouge, Marie" sort="Lagouge, Marie" uniqKey="Lagouge M" first="Marie" last="Lagouge">Marie Lagouge</name>
</noCountry>
<country name="France"><region name="Grand Est"><name sortKey="Rasouri, Soumya" sort="Rasouri, Soumya" uniqKey="Rasouri S" first="Soumya" last="Rasouri">Soumya Rasouri</name>
</region>
</country>
</tree>
</affiliations>
</record>
Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Sante/explor/ParkinsonFranceV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002586 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002586 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien |wiki= Wicri/Sante |area= ParkinsonFranceV1 |flux= Main |étape= Exploration |type= RBID |clé= pubmed:17937892 |texte= [SIRT1/PGC-1: a neuroprotective axis?]. }}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:17937892" \ | HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \ | NlmPubMed2Wicri -a ParkinsonFranceV1
![]() | This area was generated with Dilib version V0.6.29. | ![]() |