Mitochondrial DNA in somatic cells: a promising target of routine clinical tests.
Alterations of mitochondrial DNA have long been considered only from a point of view of rare genetic disorders causing neuromyopathy. Recently, alterations of mitochondrial DNA have been found in so-called common diseases such as heart failure, diabetes, and cancer; some of these alterations are inherited, and some are generated and/or accumulated in somatic cells with age. Mitochondrial DNA is more vulnerable to alteration than is nuclear DNA. For example, mitochondria produce a large amount of reactive oxygen species as an inevitable byproduct of oxidative phosphorylation. Therefore, mitochondrial DNA is under much stronger oxidative stress than is nuclear DNA. In spite of the importance, it is much less elucidated in the mitochondrial genome than in the nuclear genome how the genome is maintained. In this review, we focus on maintenance of mitochondrial DNA in somatic cells and its clinical importance.
Kang
Dongchon
D
Department of Clinical Chemistry and Laboratory Medicine, Kyushu University Graduate School of Medical Sciences, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan. kang@mailserver.med.kyushu-u.ac.jp
Hamasaki
Naotaka
N
D000818:Animals; D019963:Clinical Chemistry Tests; D004260:DNA Repair; D004261:DNA Replication; D004272:DNA, Mitochondrial / Q000187:drug effects / Q000235:genetics* / Q000378:metabolism; D003920:Diabetes Mellitus / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000378:metabolism; D009369:Neoplasms / Q000235:genetics; D019636:Neurodegenerative Diseases / Q000235:genetics; D018384:Oxidative Stress
D004272:DNA, Mitochondrial