Selective Autophagy Receptors in Neuronal Health and Disease.
Identifieur interne : 000A66 ( Ncbi/Merge ); précédent : 000A65; suivant : 000A67Selective Autophagy Receptors in Neuronal Health and Disease.
Auteurs : Owen Conway [Royaume-Uni] ; Hafize Aysin Akpinar [Royaume-Uni] ; Vladimir V. Rogov [Allemagne] ; Vladimir Kirkin [Royaume-Uni]Source :
- Journal of molecular biology [ 1089-8638 ] ; 2019.
Abstract
Neurons are electrically excitable, postmitotic cells that perform sensory, relaying, and motor functions. Because of their unique morphological and functional specialization, cells of this type are sensitive to the stress caused by accumulation of misfolded proteins or damaged organelles. Autophagy is the fundamental mechanism that ensures sequestration of cytosolic material and its subsequent degradation in lysosomes of eukaryotic cells, thereby providing cell-autonomous nutrients and removing harmful cargos. Strikingly, mice and flies lacking functional autophagy develop early onset progressive neurodegeneration. Like in human neurodegenerative diseases (NDDs)-Alzheimer's disease, Parkinson's disease, frontotemporal dementia, Huntington's disease, and amyotrophic lateral sclerosis-characteristic protein aggregates observed in autophagy-deficient neurons in the animal models are indicators of the ongoing neuronal pathology. A number of selective autophagy receptors (SARs) have been characterized that interact both with the cargo and components of the autophagic machinery, thus providing the molecular basis for selective degradation of sizable cytosolic components. Interference with autophagy in experimental models, but also during the pathological vagaries in neurons, will thus have far-reaching consequences for a range of selective autophagy pathways critical for the normal functioning of the nervous system. Here, we review the key principles behind the selective autophagy and discuss how the SARs may be involved in the pathogenesis of NDDs. Using recently published examples, we also examine the emerging role of less well studied selective autophagy pathways in neuronal health and disease. We conclude by discussing targeting selective autophagy as an emerging therapeutic modality in NDDs.
DOI: 10.1016/j.jmb.2019.10.013
PubMed: 31654670
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Rogov</name><affiliation wicri:level="4"><nlm:affiliation>Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University Frankfurt, Max-von-Laue Str. 9, 60438 Frankfurt Am Main, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University Frankfurt, Max-von-Laue Str. 9, 60438 Frankfurt Am Main</wicri:regionArea><placeName><region type="land" nuts="1">Hesse (Land)</region><region type="district" nuts="2">District de Darmstadt</region><settlement type="city">Francfort-sur-le-Main</settlement></placeName><orgName type="university">Université Johann Wolfgang Goethe de Francfort-sur-le-Main</orgName></affiliation></author><author><name sortKey="Kirkin, Vladimir" sort="Kirkin, Vladimir" uniqKey="Kirkin V" first="Vladimir" last="Kirkin">Vladimir Kirkin</name><affiliation wicri:level="1"><nlm:affiliation>Cancer Research UK Cancer Therapeutics Unit, The Institute of Cancer Research, London SM2 5NG, UK. Electronic address: vladimir.kirkin@icr.ac.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Cancer Research UK Cancer Therapeutics Unit, The Institute of Cancer Research, London SM2 5NG</wicri:regionArea><wicri:noRegion>London SM2 5NG</wicri:noRegion></affiliation></author></analytic><series><title level="j">Journal of molecular biology</title><idno type="eISSN">1089-8638</idno><imprint><date when="2019" type="published">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neurons are electrically excitable, postmitotic cells that perform sensory, relaying, and motor functions. Because of their unique morphological and functional specialization, cells of this type are sensitive to the stress caused by accumulation of misfolded proteins or damaged organelles. Autophagy is the fundamental mechanism that ensures sequestration of cytosolic material and its subsequent degradation in lysosomes of eukaryotic cells, thereby providing cell-autonomous nutrients and removing harmful cargos. Strikingly, mice and flies lacking functional autophagy develop early onset progressive neurodegeneration. Like in human neurodegenerative diseases (NDDs)-Alzheimer's disease, Parkinson's disease, frontotemporal dementia, Huntington's disease, and amyotrophic lateral sclerosis-characteristic protein aggregates observed in autophagy-deficient neurons in the animal models are indicators of the ongoing neuronal pathology. A number of selective autophagy receptors (SARs) have been characterized that interact both with the cargo and components of the autophagic machinery, thus providing the molecular basis for selective degradation of sizable cytosolic components. Interference with autophagy in experimental models, but also during the pathological vagaries in neurons, will thus have far-reaching consequences for a range of selective autophagy pathways critical for the normal functioning of the nervous system. Here, we review the key principles behind the selective autophagy and discuss how the SARs may be involved in the pathogenesis of NDDs. Using recently published examples, we also examine the emerging role of less well studied selective autophagy pathways in neuronal health and disease. We conclude by discussing targeting selective autophagy as an emerging therapeutic modality in NDDs.</div></front></TEI><pubmed><MedlineCitation Status="Publisher" Owner="NLM"><PMID Version="1">31654670</PMID><DateRevised><Year>2019</Year><Month>11</Month><Day>29</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1089-8638</ISSN><JournalIssue CitedMedium="Internet"><PubDate><Year>2019</Year><Month>Oct</Month><Day>22</Day></PubDate></JournalIssue><Title>Journal of molecular biology</Title><ISOAbbreviation>J. Mol. Biol.</ISOAbbreviation></Journal><ArticleTitle>Selective Autophagy Receptors in Neuronal Health and Disease.</ArticleTitle><ELocationID EIdType="pii" ValidYN="Y">S0022-2836(19)30609-6</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.jmb.2019.10.013</ELocationID><Abstract><AbstractText>Neurons are electrically excitable, postmitotic cells that perform sensory, relaying, and motor functions. Because of their unique morphological and functional specialization, cells of this type are sensitive to the stress caused by accumulation of misfolded proteins or damaged organelles. Autophagy is the fundamental mechanism that ensures sequestration of cytosolic material and its subsequent degradation in lysosomes of eukaryotic cells, thereby providing cell-autonomous nutrients and removing harmful cargos. Strikingly, mice and flies lacking functional autophagy develop early onset progressive neurodegeneration. Like in human neurodegenerative diseases (NDDs)-Alzheimer's disease, Parkinson's disease, frontotemporal dementia, Huntington's disease, and amyotrophic lateral sclerosis-characteristic protein aggregates observed in autophagy-deficient neurons in the animal models are indicators of the ongoing neuronal pathology. A number of selective autophagy receptors (SARs) have been characterized that interact both with the cargo and components of the autophagic machinery, thus providing the molecular basis for selective degradation of sizable cytosolic components. Interference with autophagy in experimental models, but also during the pathological vagaries in neurons, will thus have far-reaching consequences for a range of selective autophagy pathways critical for the normal functioning of the nervous system. Here, we review the key principles behind the selective autophagy and discuss how the SARs may be involved in the pathogenesis of NDDs. Using recently published examples, we also examine the emerging role of less well studied selective autophagy pathways in neuronal health and disease. We conclude by discussing targeting selective autophagy as an emerging therapeutic modality in NDDs.</AbstractText><CopyrightInformation>Copyright © 2019 Elsevier Ltd. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Conway</LastName><ForeName>Owen</ForeName><Initials>O</Initials><AffiliationInfo><Affiliation>Cancer Research UK Cancer Therapeutics Unit, The Institute of Cancer Research, London SM2 5NG, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Akpinar</LastName><ForeName>Hafize Aysin</ForeName><Initials>HA</Initials><AffiliationInfo><Affiliation>Cancer Research UK Cancer Therapeutics Unit, The Institute of Cancer Research, London SM2 5NG, UK.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rogov</LastName><ForeName>Vladimir V</ForeName><Initials>VV</Initials><AffiliationInfo><Affiliation>Institute of Biophysical Chemistry and Center for Biomolecular Magnetic Resonance, Goethe University Frankfurt, Max-von-Laue Str. 9, 60438 Frankfurt Am Main, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kirkin</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials><AffiliationInfo><Affiliation>Cancer Research UK Cancer Therapeutics Unit, The Institute of Cancer Research, London SM2 5NG, UK. Electronic address: vladimir.kirkin@icr.ac.uk.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016454">Review</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2019</Year><Month>10</Month><Day>22</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>J Mol Biol</MedlineTA><NlmUniqueID>2985088R</NlmUniqueID><ISSNLinking>0022-2836</ISSNLinking></MedlineJournalInfo><CitationSubset>IM</CitationSubset><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">Aggregates</Keyword><Keyword MajorTopicYN="N">LC3/GABARAPs</Keyword><Keyword MajorTopicYN="N">Neurodegeneration</Keyword><Keyword MajorTopicYN="N">SAR</Keyword><Keyword MajorTopicYN="N">Selective autophagy</Keyword></KeywordList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2019</Year><Month>08</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2019</Year><Month>09</Month><Day>27</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2019</Year><Month>10</Month><Day>10</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2019</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2019</Year><Month>10</Month><Day>28</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2019</Year><Month>10</Month><Day>27</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>aheadofprint</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">31654670</ArticleId><ArticleId IdType="pii">S0022-2836(19)30609-6</ArticleId><ArticleId IdType="doi">10.1016/j.jmb.2019.10.013</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Allemagne</li><li>Royaume-Uni</li></country><region><li>District de Darmstadt</li><li>Hesse (Land)</li></region><settlement><li>Francfort-sur-le-Main</li></settlement><orgName><li>Université Johann Wolfgang Goethe de Francfort-sur-le-Main</li></orgName></list><tree><country name="Royaume-Uni"><noRegion><name sortKey="Conway, Owen" sort="Conway, Owen" uniqKey="Conway O" first="Owen" last="Conway">Owen Conway</name></noRegion><name sortKey="Akpinar, Hafize Aysin" sort="Akpinar, Hafize Aysin" uniqKey="Akpinar H" first="Hafize Aysin" last="Akpinar">Hafize Aysin Akpinar</name><name sortKey="Kirkin, Vladimir" sort="Kirkin, Vladimir" uniqKey="Kirkin V" first="Vladimir" last="Kirkin">Vladimir Kirkin</name></country><country name="Allemagne"><region name="Hesse (Land)"><name sortKey="Rogov, Vladimir V" sort="Rogov, Vladimir V" uniqKey="Rogov V" first="Vladimir V" last="Rogov">Vladimir V. 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