rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2009-5-4
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pubmed:abstractText |
There is strong and consistent evidence that oxidative stress is crucially involved in the development of atherosclerotic vascular disease. Overproduction of reactive oxygen species (ROS) in mitochondria is an unifying mechanism that underlies micro- and macrovascular atherosclerotic disease. Given the central role of mitochondria in energy and ROS production, mitochondrial DNA (mtDNA) is an obvious candidate for genetic susceptibility studies on atherosclerotic processes. We therefore examined the association between mtDNA haplogroups and coronary artery disease (CAD) as well as diabetic retinopathy.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-10220377,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-10936107,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-11571560,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-12689883,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-12826641,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-12940915,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-14587078,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-14680682,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-15262184,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-15589073,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-15786469,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-15802360,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-15919781,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-16157955,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-16285865,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-16635434,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-16960846,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17033820,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17068300,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17081685,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17127367,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17306632,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17332437,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17418682,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17551080,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-17653206,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-18280061,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-18458168,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-7526212,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-9150158,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-9187202,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19383124-9538986
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:issn |
1471-2350
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pubmed:author |
pubmed-author:AignerIreneI,
pubmed-author:EderWaltraudW,
pubmed-author:HaasAntonA,
pubmed-author:IglsederBernhardB,
pubmed-author:KoflerBarbaraB,
pubmed-author:MaierRichardR,
pubmed-author:MayrJohannes AJA,
pubmed-author:MuellerEdith EEE,
pubmed-author:PaulweberBernhardB,
pubmed-author:RennerWilfriedW,
pubmed-author:SanticDanijelaD,
pubmed-author:SchmutOttoO,
pubmed-author:SperlWolfgangW,
pubmed-author:StangerOlafO,
pubmed-author:WegerMartinM,
pubmed-author:WiesbauerMartinaM,
pubmed-author:WinkerRobertR,
pubmed-author:ZimmermannFranz AFA
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pubmed:issnType |
Electronic
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pubmed:volume |
10
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
35
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:19383124-Aged,
pubmed-meshheading:19383124-Aged, 80 and over,
pubmed-meshheading:19383124-Austria,
pubmed-meshheading:19383124-Case-Control Studies,
pubmed-meshheading:19383124-Coronary Artery Disease,
pubmed-meshheading:19383124-DNA, Mitochondrial,
pubmed-meshheading:19383124-Diabetic Retinopathy,
pubmed-meshheading:19383124-Female,
pubmed-meshheading:19383124-Gene Frequency,
pubmed-meshheading:19383124-Genetic Predisposition to Disease,
pubmed-meshheading:19383124-Haplotypes,
pubmed-meshheading:19383124-Humans,
pubmed-meshheading:19383124-Male,
pubmed-meshheading:19383124-Middle Aged,
pubmed-meshheading:19383124-Odds Ratio,
pubmed-meshheading:19383124-Polymorphism, Single Nucleotide
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pubmed:year |
2009
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pubmed:articleTitle |
Mitochondrial DNA haplogroup T is associated with coronary artery disease and diabetic retinopathy: a case control study.
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pubmed:affiliation |
Department of Pediatrics, University Hospital Salzburg, Paracelsus Medical University, Salzburg, Austria. b.kofler@salk.at
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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