Mitochondrial DNA mutations and aging: A case closed?

Konstantin Khrapko; Jan Vijg

doi:10.1038/ng0407-445

Mitochondrial DNA mutations and aging: A case closed?

Konstantin Khrapko, Jan Vijg

Research output: Contribution to journal › Short survey › peer-review

44 Scopus citations

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 language	English (US)
Pages (from-to)	445-446
Number of pages	2
Journal	Nature Genetics
Volume	39
Issue number	4
DOIs	https://doi.org/10.1038/ng0407-445
State	Published - Apr 2007
Externally published	Yes

ASJC Scopus subject areas

Genetics

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10.1038/ng0407-445

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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.",

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Mitochondrial DNA mutations and aging: A case closed?

Abstract

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