[SIRT1/PGC-1: a neuroprotective axis?].
Identifieur interne : 000D13 ( PubMed/Curation ); précédent : 000D12; suivant : 000D14[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.
DOI: 10.1051/medsci/20072310840
PubMed: 17937892
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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><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">17937892</PMID><DateCreated><Year>2007</Year><Month>10</Month><Day>16</Day></DateCreated><DateCompleted><Year>2008</Year><Month>01</Month><Day>31</Day></DateCompleted><DateRevised><Year>2013</Year><Month>06</Month><Day>03</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0767-0974</ISSN><JournalIssue CitedMedium="Print"><Volume>23</Volume><Issue>10</Issue><PubDate><Year>2007</Year><Month>Oct</Month></PubDate></JournalIssue><Title>Medecine sciences : M/S</Title><ISOAbbreviation>Med Sci (Paris)</ISOAbbreviation></Journal><ArticleTitle>[SIRT1/PGC-1: a neuroprotective axis?].</ArticleTitle><Pagination><MedlinePgn>840-4</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Rasouri</LastName><ForeName>Soumya</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/Inserm/ULP, 1, rue Laurent Fries, 67404 Illkirch, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lagouge</LastName><ForeName>Marie</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Auwerx</LastName><ForeName>Johan</ForeName><Initials>J</Initials></Author></AuthorList><Language>fre</Language><PublicationTypeList><PublicationType UI="D004740">English Abstract</PublicationType><PublicationType UI="D016428">Journal 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MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011499" MajorTopicYN="N">Protein Processing, Post-Translational</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D017382" MajorTopicYN="N">Reactive Oxygen Species</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D056564" MajorTopicYN="N">Sirtuin 1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D037761" MajorTopicYN="N">Sirtuins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013267" MajorTopicYN="N">Stilbenes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName><QualifierName UI="Q000627" MajorTopicYN="N">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014157" MajorTopicYN="N">Transcription Factors</DescriptorName><QualifierName UI="Q000172" MajorTopicYN="N">deficiency</QualifierName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015533" MajorTopicYN="N">Transcriptional Activation</DescriptorName></MeshHeading></MeshHeadingList><NumberOfReferences>30</NumberOfReferences></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2007</Year><Month>10</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2008</Year><Month>2</Month><Day>1</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2007</Year><Month>10</Month><Day>17</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">17937892</ArticleId><ArticleId IdType="pii">00/00/0B/74/</ArticleId><ArticleId IdType="doi">10.1051/medsci/20072310840</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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