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dc.contributor.authorCui, Hang
dc.contributor.authorKong, Yahui
dc.contributor.authorZhang, Hong
dc.date2022-08-11T08:09:40.000
dc.date.accessioned2022-08-23T16:39:36Z
dc.date.available2022-08-23T16:39:36Z
dc.date.issued2012-10-01
dc.date.submitted2012-03-29
dc.identifier.citationJ Signal Transduct. 2012;2012:646354. Epub 2011 Oct 2. <a href="http://dx.doi.org/10.1155/2012/646354">Link to article on publisher's site</a>
dc.identifier.issn2090-1747 (Linking)
dc.identifier.doi10.1155/2012/646354
dc.identifier.pmid21977319
dc.identifier.pmid21977319
dc.identifier.urihttp://hdl.handle.net/20.500.14038/39509
dc.description.abstractAging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.
dc.language.isoen_US
dc.publisherHindawi
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=21977319&dopt=Abstract">Link to Article in PubMed</a>
dc.rights<p>Copyright © 2012 Hang Cui et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</p>
dc.subjectAging
dc.subjectReactive Oxygen Species
dc.subjectDNA, Mitochondrial
dc.subjectCell and Developmental Biology
dc.subjectCell Biology
dc.subjectPhysiology
dc.titleOxidative stress, mitochondrial dysfunction, and aging
dc.typeJournal Article
dc.source.journaltitleJournal of signal transduction
dc.source.volume2012
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=3303&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/2303
dc.identifier.contextkey2710614
refterms.dateFOA2022-08-23T16:39:36Z
html.description.abstract<p>Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.</p>
dc.identifier.submissionpathoapubs/2303
dc.contributor.departmentDepartment of Cell Biology
dc.source.pages646354


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