Mitochondrial DNA mutations and aging: A case closed?

Konstantin Khrapko, Jan Vijg

Research output: Contribution to journalArticle

41 Citations (Scopus)

Abstract

Recent reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA mutagenesis (so-called 'mitochondrial mutator mice') appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study reports that levels of point mutations in tissues of aged normal mice are much lower than in the mutator mice, apparently ruling out a causal role in normal aging.

Original languageEnglish (US)
Pages (from-to)445-446
Number of pages2
JournalNature Genetics
Volume39
Issue number4
DOIs
StatePublished - Apr 2007
Externally publishedYes

Fingerprint

Mitochondrial DNA
Mutation
Premature Aging
Point Mutation
Mutagenesis

ASJC Scopus subject areas

  • Genetics(clinical)
  • Genetics

Cite this

Mitochondrial DNA mutations and aging : A case closed? / Khrapko, Konstantin; Vijg, Jan.

In: Nature Genetics, Vol. 39, No. 4, 04.2007, p. 445-446.

Research output: Contribution to journalArticle

Khrapko, Konstantin ; Vijg, Jan. / Mitochondrial DNA mutations and aging : A case closed?. In: Nature Genetics. 2007 ; Vol. 39, No. 4. pp. 445-446.
@article{5b9a712186114a21a4f0db08f08d9be0,
title = "Mitochondrial DNA mutations and aging: A case closed?",
abstract = "Recent reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA mutagenesis (so-called 'mitochondrial mutator mice') appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study reports that levels of point mutations in tissues of aged normal mice are much lower than in the mutator mice, apparently ruling out a causal role in normal aging.",
author = "Konstantin Khrapko and Jan Vijg",
year = "2007",
month = "4",
doi = "10.1038/ng0407-445",
language = "English (US)",
volume = "39",
pages = "445--446",
journal = "Nature Genetics",
issn = "1061-4036",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - Mitochondrial DNA mutations and aging

T2 - A case closed?

AU - Khrapko, Konstantin

AU - Vijg, Jan

PY - 2007/4

Y1 - 2007/4

N2 - Recent reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA mutagenesis (so-called 'mitochondrial mutator mice') appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study reports that levels of point mutations in tissues of aged normal mice are much lower than in the mutator mice, apparently ruling out a causal role in normal aging.

AB - Recent reports of premature aging in mutant mice with greatly increased rates of mitochondrial DNA mutagenesis (so-called 'mitochondrial mutator mice') appeared to confirm that accumulation of mtDNA mutations is a key mechanism of normal aging. Now, in a dramatic turnaround, a new study reports that levels of point mutations in tissues of aged normal mice are much lower than in the mutator mice, apparently ruling out a causal role in normal aging.

UR - http://www.scopus.com/inward/record.url?scp=34047095284&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34047095284&partnerID=8YFLogxK

U2 - 10.1038/ng0407-445

DO - 10.1038/ng0407-445

M3 - Article

C2 - 17392805

AN - SCOPUS:34047095284

VL - 39

SP - 445

EP - 446

JO - Nature Genetics

JF - Nature Genetics

SN - 1061-4036

IS - 4

ER -