Mitochondrial dysfunction and mitochondrial DNA mutations in atherosclerotic complications in diabetes

Mitochondrial DNA(mtDNA) is particularly prone to oxidation due to the lack of histones and a deficient mismatch repair system.This explains an increased mutation rate of mtDNA that results in heteroplasmy,e.g.,the coexistence of the mutant and wild-type mtDNA molecules within the same mitochondrion...

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Published inWorld journal of cardiology Vol. 4; no. 5; pp. 148 - 156
Main Authors Chistiakov, Dimitry A, Sobenin, Igor A, Bobryshev, Yuri V, Orekhov, Alexander N
Format Journal Article
LanguageEnglish
Published United States Baishideng Publishing Group Co., Limited 26.05.2012
Subjects
Atherosclerosis
Diabetes
DNA
Guidelines For Basic Science
Heteroplasmy
Mitochondrial
Mutation
Oxidative
stress
Ultrastructure
Oxidative stress
Heteroplasmy
Ultrastructure
Atherosclerosis
Mitochondrial DNA
Diabetes
Mutation
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Summary:Mitochondrial DNA(mtDNA) is particularly prone to oxidation due to the lack of histones and a deficient mismatch repair system.This explains an increased mutation rate of mtDNA that results in heteroplasmy,e.g.,the coexistence of the mutant and wild-type mtDNA molecules within the same mitochondrion.In diabetes mellitus,glycotoxicity,advanced oxidative stress,collagen cross-linking,and accumulation of lipid peroxides in foam macrophage cells and arterial wall cells may significantly decrease the mutation threshold required for mitochondrial dysfunction,which in turn further contributes to the oxidative damage of the diabetic vascular wall,endothelial dysfunc-tion,and atherosclerosis.
Bibliography:Dimitry A Chistiakov,Igor A Sobenin,Department of Medical Nanobiotechnology,Pirogov Russian State Medical University,117997 Moscow,Russia Dimitry A Chistiakov,Yuri V Bobryshev,Alexander N Orekhov,Institute for Atherosclerosis Research,Skolkovo Innovative Centre,121609 Moscow,Russia Igor A Sobenin,Alexander N Orekhov,Institute of General Pathology and Pathophysiology,Russian Academy of Medical Sciences,125315 Moscow,Russia Igor A Sobenin,Russian Cardiology Research and Production Complex,121552 Moscow,Russia Yuri V Bobryshev,Faculty of Medicine,School of Medical Sciences,University of New South Wales,NSW 2052,Sydney,Australia
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Author contributions: All authors participated in conception of the topic, literature search and analysis, writing of the manuscript, and approved the final version of the manuscript.
Correspondence to: Yuri V Bobryshev, PhD, Faculty of Medicine, School of Medical Sciences, University of New South Wales, Kensington, NSW 2052, Sydney, Australia. y.bobryshev@unsw.edu.au
Telephone: +61-2-93851217 Fax: +61-2-93851217
ISSN:1949-8462
1949-8462
DOI:10.4330/wjc.v4.i5.148