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Cited 68 time in webofscience Cited 78 time in scopus
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dc.contributor.authorA-Ra-Hwang-
dc.contributor.authorDae-Eun-Jeong-
dc.contributor.authorLee, SJ-
dc.date.accessioned2016-03-31T08:51:20Z-
dc.date.available2016-03-31T08:51:20Z-
dc.date.created2016-02-15-
dc.date.issued2012-11-
dc.identifier.issn1389-2029-
dc.identifier.other2012-OAK-0000026251-
dc.identifier.urihttps://oasis.postech.ac.kr/handle/2014.oak/16182-
dc.description.abstractMitochondria are essential for various biological processes including cellular energy production. The oxidative stress theory of aging proposes that mitochondria play key roles in aging by generating reactive oxygen species (ROS), which indiscriminately damage macromolecules and lead to an age-dependent decline in biological function. However, recent studies show that increased levels of ROS or inhibition of mitochondrial function can actually delay aging and increase lifespan. The aim of this review is to summarize recent findings regarding the role of mitochondria in organismal aging processes. We will discuss how mitochondria contribute to evolutionarily conserved longevity pathways, including mild inhibition of respiration, dietary restriction, and target of rapamycin (TOR) signaling.-
dc.description.statementofresponsibilityX-
dc.languageEnglish-
dc.publisherBentham Science-
dc.relation.isPartOfCURRENT GENOMICS-
dc.subjectMitochondria-
dc.subjectAging-
dc.subjectReactive oxygen species-
dc.subjectDietary restriction-
dc.subjectTarget of rapamycin (TOR)-
dc.subjectLIFE-SPAN EXTENSION-
dc.subjectHYPOXIA-INDUCIBLE FACTOR-
dc.subjectTRANSCRIPTIONAL COACTIVATOR PGC-1-ALPHA-
dc.subjectNEMATODE CAENORHABDITIS-ELEGANS-
dc.subjectRESTRICTION-INDUCED LONGEVITY-
dc.subjectOXYGEN SPECIES GENERATION-
dc.subjectELECTRON-TRANSPORT CHAIN-
dc.subjectGENE-EXPRESSION PROFILE-
dc.subjectFEMALE SHR MICE-
dc.subjectCALORIE RESTRICTION-
dc.titleMitochondria and Organismal Longevity-
dc.typeArticle-
dc.contributor.college정보전자융합공학부-
dc.identifier.doi10.2174/138920212803251427-
dc.author.googleHwang, AB-
dc.author.googleJeong, DE-
dc.author.googleLee, SJ-
dc.relation.volume13-
dc.relation.issue7-
dc.relation.startpage519-
dc.relation.lastpage532-
dc.contributor.id10201212-
dc.relation.journalCURRENT GENOMICS-
dc.relation.indexSCI급, SCOPUS 등재논문-
dc.collections.nameJournal Papers-
dc.type.rimsART-
dc.identifier.bibliographicCitationCURRENT GENOMICS, v.13, no.7, pp.519 - 532-
dc.identifier.wosid000309545300004-
dc.date.tcdate2019-01-01-
dc.citation.endPage532-
dc.citation.number7-
dc.citation.startPage519-
dc.citation.titleCURRENT GENOMICS-
dc.citation.volume13-
dc.contributor.affiliatedAuthorLee, SJ-
dc.identifier.scopusid2-s2.0-84867756222-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.wostc32-
dc.type.docTypeArticle-
dc.subject.keywordPlusLIFE-SPAN EXTENSION-
dc.subject.keywordPlusHYPOXIA-INDUCIBLE FACTOR-
dc.subject.keywordPlusGENE-EXPRESSION PROFILE-
dc.subject.keywordPlusRESTRICTION-INDUCED LONGEVITY-
dc.subject.keywordPlusOXYGEN SPECIES GENERATION-
dc.subject.keywordPlusELECTRON-TRANSPORT CHAIN-
dc.subject.keywordPlusCALORIE RESTRICTION-
dc.subject.keywordPlusCAENORHABDITIS-ELEGANS-
dc.subject.keywordPlusDIETARY RESTRICTION-
dc.subject.keywordPlusOXIDATIVE-PHOSPHORYLATION-
dc.subject.keywordAuthorMitochondria-
dc.subject.keywordAuthorAging-
dc.subject.keywordAuthorReactive oxygen species-
dc.subject.keywordAuthorDietary restriction-
dc.subject.keywordAuthorTarget of rapamycin (TOR)-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryGenetics & Heredity-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaGenetics & Heredity-

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이승재LEE, SEUNG JAE
Dept of Life Sciences
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