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dc.contributor.authorTerman, A
dc.contributor.authorDalen, H
dc.contributor.authorEaton, JW
dc.contributor.authorNeuzil, J
dc.contributor.authorBrunka, UT
dc.contributor.editorDeGrey, ADN
dc.date.accessioned2017-05-03T12:22:18Z
dc.date.available2017-05-03T12:22:18Z
dc.date.issued2004
dc.date.modified2009-09-08T08:03:55Z
dc.identifier.issn0077-8923
dc.identifier.doi10.1196/annals.1297.015
dc.identifier.urihttp://hdl.handle.net/10072/5504
dc.description.abstractOxidative stress is believed to be an important contributor to aging, mainly affecting long-lived postmitotic cells such as cardiac myocytes and neurons. Aging cells accumulate functionally effete, often mutant and enlarged mitochondria, as well as an intralysosomal undegradable pigment, lipofuscin. To provide better insight into the role of oxidative stress, mitochondrial damage, and lipofuscinogenesis in postmitotic aging, we studied the relationship between these parameters in cultured neonatal rat cardiac myocytes. It was found that the content of lipofuscin, which varied drastically between cells, positively correlated with mitochondrial damage (evaluated by decreased innermembrane potential), as well as with the production of reactive oxygen species. These results suggest that both lipofuscin accumulation and mitochondrial damage have common underlying mechanisms, likely including imperfect autophagy and ensuing lysosomal degradation of oxidatively damaged mitochondria and other organelles. Increased size of mitochondria (possibly resulting from impaired fission due to oxidative damage to mitochondrial DNA, membranes, and proteins) also may interfere with mitochondrial turnover, leading to the appearance of so-called "giant" mitochondria. This assumption is based on our observation that pharmacological inhibition of autophagy with 3-methyladenine induced only moderate accumulation of large (senescent-like) mitochondria but drastically increased numbers of small, apparently normal mitochondria, reflecting their rapid turnover and suggesting that enlarged mitochondria are poorly autophagocytosed. Overall, our findings emphasize the importance of mitochondrial turnover in postmitotic aging and provide further support for the mitochondrial-lysosomal axis theory of aging.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherNew York Academy of Sciences
dc.publisher.placeUnited States
dc.publisher.urihttps://nyaspubs.onlinelibrary.wiley.com/doi/10.1196/annals.1297.015
dc.relation.ispartofpagefrom70
dc.relation.ispartofpageto77
dc.relation.ispartofjournalNew York Academy of Sciences, Annals
dc.relation.ispartofvolume1019
dc.subject.fieldofresearchcode270106
dc.titleAging of cardiac myocytes in culture: oxidative stress, lipofuscin accumulation, and mitochondrial turnover
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
gro.rights.copyright© 2004 Wiley-Blackwell Publishing. The definitive version is available at www.interscience.wiley.com
gro.date.issued2004
gro.hasfulltextNo Full Text
gro.griffith.authorNeuzil, Jiri


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