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dc.contributor.authorBennett, Martin
dc.contributor.authorYu, Emma
dc.contributor.authorFoote, Kirsty
dc.date.accessioned2018-09-08T06:32:01Z
dc.date.available2018-09-08T06:32:01Z
dc.date.issued2018-11-01
dc.identifier.issn0008-6363
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/279837
dc.description.abstractMitochondria contain multiple copies of mitochondrial DNA (mtDNA) that encode ribosomal and transfer RNAs and many essential proteins required for oxidative phosphorylation. Mitochondria are essential for generation of ATP, but also generate reactive oxygen species (ROS) as a by-product of the electron transport chain. Oxidative damage to mitochondrial DNA induces respiratory chain dysfunction, resulting in reduced ATP synthesis and further increased ROS generation. The reduced mitochondrial respiration may be accompanied by increased glycolysis and increased lactate production, and these changes can be detected by reduced oxygen consumption and increased extracellular pH of tissues or cultured cells. Mitochondrial dysfunction leading to reduced mitochondrial respiration has been implicated in both normal vascular ageing and a variety of cardiovascular diseases,, including atherosclerosis, heart failure, and aneurysm formation. For example, reduced mitochondrial DNA (mtDNA) copy number, mitochondrial respiration and expression of specific electron transport chain complexes has been shown in vascular smooth muscle cells (VSMCs) derived from human atherosclerotic plaques1-3. Mitochondriogenesis and mitophagy are also important regulators of mitochondrial health and number. ROS induce VSMC mitophagy, and similarly plaque VSMCs show increased mitophagy compared with normal arterial VSMCs2.
dc.description.sponsorshipThis work was supported by British Heart Foundation (BHF) grants PG/14/69/31032 and RG/13/14/30314, the National Institute for Health Research Cambridge Biomedical Research Centre, the BHF Centre for Research Excellence, the Academy of Medical Sciences.
dc.publisherOxford University Press
dc.titleMitochondrial function in thoracic aortic aneurysms
dc.typeArticle
prism.publicationNameCardiovascular Research
dc.identifier.doi10.17863/CAM.27205
dcterms.dateAccepted2018-07-04
rioxxterms.versionofrecord10.1093/cvr/cvy180
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
rioxxterms.licenseref.startdate2018-07-04
dc.contributor.orcidBennett, Martin [0000-0002-2565-1825]
dc.identifier.eissn1755-3245
rioxxterms.typeJournal Article/Review
pubs.funder-project-idBritish Heart Foundation (None)
pubs.funder-project-idBritish Heart Foundation (None)
pubs.funder-project-idBritish Heart Foundation (None)
pubs.funder-project-idBritish Heart Foundation (PG/16/11/32021)
pubs.funder-project-idBritish Heart Foundation (PG/16/63/32307)
pubs.funder-project-idBritish Heart Foundation (CH/2000003)
pubs.funder-project-idBritish Heart Foundation (PG/16/24/32090)
pubs.funder-project-idBritish Heart Foundation (None)
cam.issuedOnline2018-07-06
rioxxterms.freetoread.startdate2019-07-06


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