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dc.contributor.authorShah, Aartien
dc.contributor.authorBennett, Martinen
dc.date.accessioned2016-09-22T10:01:57Z
dc.date.available2016-09-22T10:01:57Z
dc.date.issued2016-09-02en
dc.identifier.issn0009-7330
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/260306
dc.description.abstractAdvanced atherosclerotic plaques demonstrate extensive DNA damage, seen in smooth muscle cells, endothelial cells, macrophages and in circulating cells, and in both nuclei and mitochondria.$^1$ DNA damage includes both single- or double-stranded breaks, deleted sections of DNA, nucleotide modifications, and extrusions of DNA from the nucleus (micronuclei). Reactive oxygen species (ROS) induce a variety of DNA damage, including oxidatively modified bases, apurinic/apyrimidinic sites, and strand breaks. Guanine is the most readily oxidized base, reacting with $^•$OH to generate a reducing neutral radical that reacts with O$_2$, and via electron transfer, forms 8-oxo-7,8-dihydroguanine (8-oxo-G).$^2$ 8-oxo-G and its products are the most abundant DNA lesions on oxidative exposure, with 1 to 2/10$^6$ residues in nuclear DNA and 1 to 3/10$^5$ residues in mitochondrial DNA (mtDNA), and up to 10$^5$ 8-oxo-G lesions are formed in the cell daily.$^1$ Advanced plaques are characterized by extensive accumulation of 8-oxo-G, seen in both macrophages and smooth muscle cells.$^{3,4}$ 8-oxo-G is primarily repaired by base excision repair by several enzymes, including specific 8-oxo-G DNA glycosylases I$^5$ and II$^6$ (OGG1/2) and the Nei-like (NEIL) glycosylases; the excised DNA is repaired by AP endonucleases before gap filling by polymerases and ligation.
dc.description.sponsorshipBritish Heart Foundation (Grant ID: RG/13/14/30314), Cambridge NIHR Biomedical Research Centre
dc.languageEnglishen
dc.language.isoenen
dc.publisherAmerican Heart Association
dc.subjectediorialsen
dc.subjectatherosclerosisen
dc.subjectDNA damageen
dc.subjectmicroRNAen
dc.subjectoxidative stressen
dc.subjectreactive oxygen speciesen
dc.titleControlling Inflammation Through DNA Damage and Repairen
dc.typeArticle
dc.description.versionThis is the author accepted manuscript. The final version is available from the American Heart Association via http://dx.doi.org/10.1161/CIRCRESAHA.116.309505en
prism.endingPage700
prism.publicationDate2016en
prism.publicationNameCirculation Researchen
prism.startingPage698
prism.volume119en
dc.identifier.doi10.17863/CAM.4537
dcterms.dateAccepted2016-07-19en
rioxxterms.versionofrecord10.1161/CIRCRESAHA.116.309505en
rioxxterms.versionAMen
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserveden
rioxxterms.licenseref.startdate2016-09-02en
dc.contributor.orcidBennett, Martin [0000-0002-2565-1825]
dc.identifier.eissn1524-4571
rioxxterms.typeJournal Article/Reviewen
pubs.funder-project-idBritish Heart Foundation (PG/16/11/32021)
pubs.funder-project-idBritish Heart Foundation (PG/11/57/29003)
pubs.funder-project-idBritish Heart Foundation (PG/13/25/30014)
pubs.funder-project-idBritish Heart Foundation (RG/13/14/30314)
rioxxterms.freetoread.startdate2017-03-02


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