Balance is the challenge – The impact of mitochondrial dynamics in Parkinson’s disease
Identifieur interne : 000C20 ( Main/Corpus ); précédent : 000C19; suivant : 000C21Balance is the challenge – The impact of mitochondrial dynamics in Parkinson’s disease
Auteurs : Lena F. Burbulla ; Guido Krebiehl ; Rejko KrügerSource :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 2010-11.
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Abstract
Eur J Clin Invest 2010; 40 (11): 1048–1060 Abstract: Impaired mitochondrial function has been implicated in neurodegeneration in Parkinson’s disease (PD) based on biochemical and pathoanatomical studies in brains of PD patients. This observation was further substantiated by the identification of exogenic toxins, i.e. complex I inhibitors that directly affect mitochondrial energy metabolism and cause Parkinsonism in humans and various animal models. Recently, insights into the underlying molecular signalling pathways leading to alterations in mitochondrial homeostasis were gained based on the functional characterization of mitoprotective genes identified in rare forms of inherited PD. Using in vitro and in vivo loss of function models of the Parkin, PINK1, DJ‐1 and Omi/HtrA2 gene, the emerging field of mitochondrial dynamics in PD was established as being critical for the maintenance of mitochondrial function in neurons. This underscored the concept that mitochondria are highly dynamic organelles, which are tightly regulated to continuously adapt shape to functional and anatomical requirements during axonal transport, synaptic signalling, organelle degradation and cellular energy supply. The dissection of pathways involved in mitochondrial quality control clearly established the PINK1/Parkin‐pathway in the clearance of dysfunctional mitochondria by autophagy and hints to a complex interplay between PD‐associated proteins acting at the mitochondrial interface. The elucidation of this mitoprotective signalling network may help to define novel therapeutic targets for PD via molecular modelling of mitochondria and/or pharmacological modulation of mitochondrial dynamics.
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DOI: 10.1111/j.1365-2362.2010.02354.x
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This observation was further substantiated by the identification of exogenic toxins, i.e. complex I inhibitors that directly affect mitochondrial energy metabolism and cause Parkinsonism in humans and various animal models. Recently, insights into the underlying molecular signalling pathways leading to alterations in mitochondrial homeostasis were gained based on the functional characterization of mitoprotective genes identified in rare forms of inherited PD. Using in vitro and in vivo loss of function models of the Parkin, PINK1, DJ‐1 and Omi/HtrA2 gene, the emerging field of mitochondrial dynamics in PD was established as being critical for the maintenance of mitochondrial function in neurons. This underscored the concept that mitochondria are highly dynamic organelles, which are tightly regulated to continuously adapt shape to functional and anatomical requirements during axonal transport, synaptic signalling, organelle degradation and cellular energy supply. The dissection of pathways involved in mitochondrial quality control clearly established the PINK1/Parkin‐pathway in the clearance of dysfunctional mitochondria by autophagy and hints to a complex interplay between PD‐associated proteins acting at the mitochondrial interface. The elucidation of this mitoprotective signalling network may help to define novel therapeutic targets for PD via molecular modelling of mitochondria and/or pharmacological modulation of mitochondrial dynamics.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Lena F. 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The dissection of pathways involved in mitochondrial quality control clearly established the PINK1/Parkin‐pathway in the clearance of dysfunctional mitochondria by autophagy and hints to a complex interplay between PD‐associated proteins acting at the mitochondrial interface. 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The dissection of pathways involved in mitochondrial quality control clearly established the PINK1/Parkin‐pathway in the clearance of dysfunctional mitochondria by autophagy and hints to a complex interplay between PD‐associated proteins acting at the mitochondrial interface. The elucidation of this mitoprotective signalling network may help to define novel therapeutic targets for PD via molecular modelling of mitochondria and/or pharmacological modulation of mitochondrial dynamics.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Autophagy</term></item><item><term>fission</term></item><item><term>fusion</term></item><item><term>mitochondria</term></item><item><term>neurodegeneration</term></item><item><term>Parkinson’s disease</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2010-11">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/DA0A5453AF1696F8BF91F0929F053013E1F46A5D/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Ltd</publisherName><publisherLoc>Oxford, UK</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1365-2362</doi><issn type="print">0014-2972</issn><issn type="electronic">1365-2362</issn><idGroup><id type="product" value="ECI"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="EUROPEAN JOURNAL OF CLINICAL INVESTIGATION">European Journal of Clinical Investigation</title></titleGroup></publicationMeta><publicationMeta level="part" position="11111"><doi origin="wiley">10.1111/eci.2010.40.issue-11</doi><numberingGroup><numbering type="journalVolume" number="40">40</numbering><numbering type="journalIssue" number="11">11</numbering></numberingGroup><coverDate startDate="2010-11">November 2010</coverDate></publicationMeta><publicationMeta level="unit" type="reviewArticle" position="11" status="forIssue"><doi origin="wiley">10.1111/j.1365-2362.2010.02354.x</doi><idGroup><id type="unit" value="ECI2354"></id></idGroup><countGroup><count type="pageTotal" number="13"></count></countGroup><titleGroup><title type="tocHeading1">REVIEWS</title></titleGroup><copyright>© 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation</copyright><eventGroup><event type="firstOnline" date="2010-08-03"></event><event type="publishedOnlineFinalForm" date="2010-08-03"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.22 mode:FullText" date="2010-10-08"></event><event type="publishedOnlineEarlyUnpaginated" date="2010-08-03"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-01-20"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-16"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="1048">1048</numbering><numbering type="pageLast" number="1060">1060</numbering></numberingGroup><correspondenceTo>Professor Dr. Rejko Krüger, MD, Laboratory of Functional Neurogenomics, Center of Neurology, Hertie‐Institute for Clinical Brain Research and German Research Center for Neurogenerative Diseases (DZNE), Hoppe‐Seyler‐Str. 3, 72076 Tübingen, Germany. Tel.: +49‐7071‐2982141; fax: +49‐7071‐295260; e‐mail: <email normalForm="rejko.krueger@uni-tuebingen.de">rejko.krueger@uni‐tuebingen.de</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:ECI.ECI2354.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 28 April 2010; accepted 28 June 2010</unparsedEditorialHistory><countGroup><count type="figureTotal" number="3"></count><count type="tableTotal" number="1"></count></countGroup><titleGroup><title type="main">Balance is the challenge – The impact of mitochondrial dynamics in Parkinson’s disease</title><title type="shortAuthors">L. F. BURBULLA <i>ET AL.</i></title><title type="short">BALANCE IS THE CHALLENGE</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2 #a3"><personName><givenNames>Lena F.</givenNames><familyName>Burbulla</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1 #a2"><personName><givenNames>Guido</givenNames><familyName>Krebiehl</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1 #a2"><personName><givenNames>Rejko</givenNames><familyName>Krüger</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="DE"><unparsedAffiliation>Department of Neurodegenerative Diseases, Hertie‐Institute for Clinical Brain Research, University of Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="DE"><unparsedAffiliation>DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="DE"><unparsedAffiliation>Graduate School of Cellular & Molecular Neuroscience, University of Tübingen, Germany</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">Autophagy</keyword><keyword xml:id="k2">fission</keyword><keyword xml:id="k3">fusion</keyword><keyword xml:id="k4">mitochondria</keyword><keyword xml:id="k5">neurodegeneration</keyword><keyword xml:id="k6">Parkinson’s disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><section xml:id="sec-sum-1"><p>Eur J Clin Invest 2010; 40 (11): 1048–1060</p></section><section xml:id="abs1-1"><title type="main">Abstract</title><p>Impaired mitochondrial function has been implicated in neurodegeneration in Parkinson’s disease (PD) based on biochemical and pathoanatomical studies in brains of PD patients. This observation was further substantiated by the identification of exogenic toxins, i.e. complex I inhibitors that directly affect mitochondrial energy metabolism and cause Parkinsonism in humans and various animal models. Recently, insights into the underlying molecular signalling pathways leading to alterations in mitochondrial homeostasis were gained based on the functional characterization of mitoprotective genes identified in rare forms of inherited PD. Using <i>in vitro</i> and <i>in vivo</i> loss of function models of the Parkin, PINK1, DJ‐1 and Omi/HtrA2 gene, the emerging field of mitochondrial dynamics in PD was established as being critical for the maintenance of mitochondrial function in neurons. This underscored the concept that mitochondria are highly dynamic organelles, which are tightly regulated to continuously adapt shape to functional and anatomical requirements during axonal transport, synaptic signalling, organelle degradation and cellular energy supply. The dissection of pathways involved in mitochondrial quality control clearly established the PINK1/Parkin‐pathway in the clearance of dysfunctional mitochondria by autophagy and hints to a complex interplay between PD‐associated proteins acting at the mitochondrial interface. The elucidation of this mitoprotective signalling network may help to define novel therapeutic targets for PD via molecular modelling of mitochondria and/or pharmacological modulation of mitochondrial dynamics.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Balance is the challenge – The impact of mitochondrial dynamics in Parkinson’s disease</title></titleInfo><titleInfo type="abbreviated"><title>BALANCE IS THE CHALLENGE</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Balance is the challenge – The impact of mitochondrial dynamics in Parkinson’s disease</title></titleInfo><name type="personal"><namePart type="given">Lena F.</namePart><namePart type="family">Burbulla</namePart><affiliation>Department of Neurodegenerative Diseases, Hertie‐Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation><affiliation>DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany</affiliation><affiliation>Graduate School of Cellular & Molecular Neuroscience, University of Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Guido</namePart><namePart type="family">Krebiehl</namePart><affiliation>Department of Neurodegenerative Diseases, Hertie‐Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation><affiliation>DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rejko</namePart><namePart type="family">Krüger</namePart><affiliation>Department of Neurodegenerative Diseases, Hertie‐Institute for Clinical Brain Research, University of Tübingen, Germany</affiliation><affiliation>DZNE, German Center for Neurodegenerative Diseases, Tübingen, Germany</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="reviewArticle"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2010-11</dateIssued><edition>Received 28 April 2010; accepted 28 June 2010</edition><copyrightDate encoding="w3cdtf">2010</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">3</extent><extent unit="tables">1</extent></physicalDescription><abstract lang="en">Eur J Clin Invest 2010; 40 (11): 1048–1060 Abstract: Impaired mitochondrial function has been implicated in neurodegeneration in Parkinson’s disease (PD) based on biochemical and pathoanatomical studies in brains of PD patients. This observation was further substantiated by the identification of exogenic toxins, i.e. complex I inhibitors that directly affect mitochondrial energy metabolism and cause Parkinsonism in humans and various animal models. Recently, insights into the underlying molecular signalling pathways leading to alterations in mitochondrial homeostasis were gained based on the functional characterization of mitoprotective genes identified in rare forms of inherited PD. Using in vitro and in vivo loss of function models of the Parkin, PINK1, DJ‐1 and Omi/HtrA2 gene, the emerging field of mitochondrial dynamics in PD was established as being critical for the maintenance of mitochondrial function in neurons. This underscored the concept that mitochondria are highly dynamic organelles, which are tightly regulated to continuously adapt shape to functional and anatomical requirements during axonal transport, synaptic signalling, organelle degradation and cellular energy supply. The dissection of pathways involved in mitochondrial quality control clearly established the PINK1/Parkin‐pathway in the clearance of dysfunctional mitochondria by autophagy and hints to a complex interplay between PD‐associated proteins acting at the mitochondrial interface. The elucidation of this mitoprotective signalling network may help to define novel therapeutic targets for PD via molecular modelling of mitochondria and/or pharmacological modulation of mitochondrial dynamics.</abstract><subject lang="en"><genre>Keywords</genre><topic>Autophagy</topic><topic>fission</topic><topic>fusion</topic><topic>mitochondria</topic><topic>neurodegeneration</topic><topic>Parkinson’s disease</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Clinical Investigation</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0014-2972</identifier><identifier type="eISSN">1365-2362</identifier><identifier type="DOI">10.1111/(ISSN)1365-2362</identifier><identifier type="PublisherID">ECI</identifier><part><date>2010</date><detail type="volume"><caption>vol.</caption><number>40</number></detail><detail type="issue"><caption>no.</caption><number>11</number></detail><extent unit="pages"><start>1048</start><end>1060</end><total>13</total></extent></part></relatedItem><identifier type="istex">DA0A5453AF1696F8BF91F0929F053013E1F46A5D</identifier><identifier type="DOI">10.1111/j.1365-2362.2010.02354.x</identifier><identifier type="ArticleID">ECI2354</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2010 The Authors. European Journal of Clinical Investigation © 2010 Stichting European Society for Clinical Investigation Journal Foundation</accessCondition><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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