Mitochondrial DNA Mutations, Oxidative Stress, and Apoptosis in Mammalian Aging
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Abstract
Mutations in mitochondrial DNA (mtDNA) accumulate in tissues of mammalian species and have been hypothesized to contribute to aging. We show that mice expressing a proofreading-deficient version of the mitochondrial DNA polymerase g (POLG) accumulate mtDNA mutations and display features of accelerated aging. Accumulation of mtDNA mutations was not associated with increased markers of oxidative stress or a defect in cellular proliferation, but was correlated with the induction of apoptotic markers, particularly in tissues characterized by rapid cellular turnover. The levels of apoptotic markers were also found to increase during aging in normal mice. Thus, accumulation of mtDNA mutations that promote apoptosis may be a central mechanism driving mammalian aging.
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The record
- Venue
- Science
- Topic
- Mitochondrial Function and Pathology
- Field
- Biochemistry, Genetics and Molecular Biology
- Canadian institutions
- Institute of Aging
- Funders
- National Institute of Diabetes and Digestive and Kidney DiseasesNational Center for Research ResourcesNational Institute of General Medical SciencesNational Institute on Aging
- Keywords
- Mitochondrial DNABiologyOxidative stressMitochondrionMutationApoptosisGeneticsDNA damageCell biologyDNA repairMolecular biologyDNAOxidative phosphorylationPolymeraseGeneBiochemistry
- Has abstract in OpenAlex
- yes