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Article: Age-related decline in stress responses of human myocardium may not be explained by changes in mtDNA

TitleAge-related decline in stress responses of human myocardium may not be explained by changes in mtDNA
Authors
KeywordsAgeing
Mitochondrial DNA
mtDNA
Myocardium
Issue Date2009
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/mechagedev
Citation
Mechanisms Of Ageing And Development, 2009, v. 130 n. 11-12, p. 742-747 How to Cite?
AbstractElderly patients undergoing cardiac surgery are more likely to suffer postoperative heart failure than younger patients. This phenomenon is mirrored by an age-related loss of mitochondrial function and by an in vitro loss of myocardial contractile force following a stress. To examine the possibility that loss of mtDNA integrity may be responsible, we quantified representative age-associated mtDNA mutations (mtDNA 4977 and mtDNA A3243G) and mtDNA copy number using quantitative polymerase chain reaction in atrial samples obtained during cardiac surgery. The myocardium underwent organ bath contractility testing before and after either an ischaemic or hypoxic stress. We found that with age, recovery of developed force after either stressor significantly declined (p < 0.0001). The abundance of mtDNA 4977 correlated weakly with loss of contractility (R 2 = 0.09, p = 0.047). However, the abundance level was low (average 0.0075% of total mtDNA) and the correlation disappeared when age was included in a multivariate analysis. Neither the abundance of mtDNA A3243G nor mtDNA copy number correlated with reduced recovery of developed force after stress. We conclude that, although mtDNA mutations (as exemplified by mtDNA 4977) accumulate in the ageing heart, they are unlikely to make a major contribution to loss of contractile function. © 2009 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/125632
ISSN
2015 Impact Factor: 2.892
2015 SCImago Journal Rankings: 1.737
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMiller, Fen_HK
dc.contributor.authorNagley, Pen_HK
dc.contributor.authorMariani, JAen_HK
dc.contributor.authorOu, Ren_HK
dc.contributor.authorLiu, VWSen_HK
dc.contributor.authorZhang, Cen_HK
dc.contributor.authorLinnane, AWen_HK
dc.contributor.authorPepe, Sen_HK
dc.contributor.authorRosenfeldt, Fen_HK
dc.date.accessioned2010-10-31T11:42:39Z-
dc.date.available2010-10-31T11:42:39Z-
dc.date.issued2009en_HK
dc.identifier.citationMechanisms Of Ageing And Development, 2009, v. 130 n. 11-12, p. 742-747en_HK
dc.identifier.issn0047-6374en_HK
dc.identifier.urihttp://hdl.handle.net/10722/125632-
dc.description.abstractElderly patients undergoing cardiac surgery are more likely to suffer postoperative heart failure than younger patients. This phenomenon is mirrored by an age-related loss of mitochondrial function and by an in vitro loss of myocardial contractile force following a stress. To examine the possibility that loss of mtDNA integrity may be responsible, we quantified representative age-associated mtDNA mutations (mtDNA 4977 and mtDNA A3243G) and mtDNA copy number using quantitative polymerase chain reaction in atrial samples obtained during cardiac surgery. The myocardium underwent organ bath contractility testing before and after either an ischaemic or hypoxic stress. We found that with age, recovery of developed force after either stressor significantly declined (p < 0.0001). The abundance of mtDNA 4977 correlated weakly with loss of contractility (R 2 = 0.09, p = 0.047). However, the abundance level was low (average 0.0075% of total mtDNA) and the correlation disappeared when age was included in a multivariate analysis. Neither the abundance of mtDNA A3243G nor mtDNA copy number correlated with reduced recovery of developed force after stress. We conclude that, although mtDNA mutations (as exemplified by mtDNA 4977) accumulate in the ageing heart, they are unlikely to make a major contribution to loss of contractile function. © 2009 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/mechagedeven_HK
dc.relation.ispartofMechanisms of Ageing and Developmenten_HK
dc.subjectAgeingen_HK
dc.subjectMitochondrial DNAen_HK
dc.subjectmtDNAen_HK
dc.subjectMyocardiumen_HK
dc.subject.meshAdolescent-
dc.subject.meshAging - physiology-
dc.subject.meshDNA, Mitochondrial - analysis - genetics-
dc.subject.meshMyocardial Contraction - physiology-
dc.subject.meshMyocardium - chemistry-
dc.titleAge-related decline in stress responses of human myocardium may not be explained by changes in mtDNAen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0047-6374&volume=130&issue=11-12&spage=742&epage=747&date=2009&atitle=Age-related+decline+in+stress+responses+of+human+myocardium+may+not+be+explained+by+changes+in+mtDNA-
dc.identifier.emailLiu, VWS: vwsliu@hkusua.hku.hken_HK
dc.identifier.authorityLiu, VWS=rp00341en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.mad.2009.09.003en_HK
dc.identifier.pmid19819254-
dc.identifier.scopuseid_2-s2.0-72149094056en_HK
dc.identifier.hkuros174901en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-72149094056&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume130en_HK
dc.identifier.issue11-12en_HK
dc.identifier.spage742en_HK
dc.identifier.epage747en_HK
dc.identifier.isiWOS:000273864900004-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridMiller, F=7401770749en_HK
dc.identifier.scopusauthoridNagley, P=7006184213en_HK
dc.identifier.scopusauthoridMariani, JA=7005470622en_HK
dc.identifier.scopusauthoridOu, R=7003500495en_HK
dc.identifier.scopusauthoridLiu, VWS=7006405113en_HK
dc.identifier.scopusauthoridZhang, C=15319862400en_HK
dc.identifier.scopusauthoridLinnane, AW=7005217117en_HK
dc.identifier.scopusauthoridPepe, S=7006204153en_HK
dc.identifier.scopusauthoridRosenfeldt, F=7006760881en_HK
dc.identifier.citeulike5923090-

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