ArticleProceedings of the National Academy of Sciences of the United States of America2003
Age-dependent deficiency in import of mitochondrial DNA glycosylases required for repair of oxidatively damaged bases.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 123 citations in OpenAlex.
- DNA repair enzymes in sunscreens and their impact on photoageing-A systematic review.Photodermatology, photoimmunology & photomedicine · 2020Pooled it
- Advances in gene therapy for mitochondrial genetic disorders: current status and clinical implementation challenges.Journal of translational medicine · 2025Review
- Molecular Duality of OGG1: From Genomic Guardian to Redox-Sensitive Modulator in Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Catalytic activity of OGG1 is impaired by Zinc deficiency.DNA repair · 2024Article
- Base Excision DNA Repair in Plants:International journal of molecular sciences · 2023Review
- Mitochondrial OGG1 expression reduces age-associated neuroinflammation by regulating cytosolic mitochondrial DNA.Free radical biology & medicine · 2023Article
- Oxidative stress induces Z-DNA-binding protein 1-dependent activation of microglia via mtDNA released from retinal pigment epithelial cells.The Journal of biological chemistry · 2022Article
- Stem Cells of the Aging Brain.Frontiers in aging neuroscience · 2020Review
- Mitochondria in the signaling pathways that control longevity and health span.Ageing research reviews · 2019Review
- mPOS is a novel mitochondrial trigger of cell death - implications for neurodegeneration.FEBS letters · 2018Review
- miR-200a Modulates the Expression of the DNA Repair Protein OGG1 Playing a Role in Aging of Primary Human Keratinocytes.Oxidative medicine and cellular longevity · 2018Article
- 8-Oxoguanine DNA glycosylase1-driven DNA repair-A paradoxical role in lung aging.Mechanisms of ageing and development · 2017Article
- SIRT6 rescues the age related decline in base excision repair in a PARP1-dependent manner.Cell cycle (Georgetown, Tex.) · 2015Article
- Inter-individual variation in DNA repair capacity: a need for multi-pathway functional assays to promote translational DNA repair research.DNA repair · 2014Article
- Overexpression of DNA ligase III in mitochondria protects cells against oxidative stress and improves mitochondrial DNA base excision repair.DNA repair · 2014Article
- mtDNA Mutations and Their Role in Aging, Diseases and Forensic Sciences.Aging and disease · 2013Review
- 8-Oxoguanine DNA glycosylase-1 links DNA repair to cellular signaling via the activation of the small GTPase Rac1.Free radical biology & medicine · 2013Article
- Tumor-derived hydrogen sulfide, produced by cystathionine-β-synthase, stimulates bioenergetics, cell proliferation, and angiogenesis in colon cancer.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Mitochondria as a target of environmental toxicants.Toxicological sciences : an official journal of the Society of Toxicology · 2013Review
- The role of mitochondrial DNA mutations and free radicals in disease and ageing.Journal of internal medicine · 2013Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The mitochondria are the major source of chronic oxidative stress, which has been implicated in the aging process. Along with other cellular changes, aged cells accumulate mutations in both their nuclear and mitochondrial genomes, and they contain increased amounts of oxidatively damaged mutagenic bases such as 7,8-dihydro-8-oxoguanine, suggesting age-dependent inhibition of its repair. Surprisingly, the level and activity of 8-oxoguanine-DNA glycosylase (OGG1), responsible for repair of 7,8-dihydro-8-oxoguanine, was found to be higher in the liver mitochondrial extract from old rodents than in that from young ones. We addressed this paradox by analyzing OGG1 in the mitochondria of young vs. old mouse livers, as well as in replicating vs. presenescent human fibroblasts. We show here that although the total OGG1 activity is higher in old mitochondria, a large fraction of the enzyme is stuck to the membrane in the precursor form, which could not be translocated to and processed in the mitochondrial matrix. A nearly identical phenomenon was observed with the mitochondrial uracil-DNA glycosylase responsible for repair of mutagenic uracil. These results indicate an age-dependent decline in the mitochondrial import of proteins needed for DNA repair and possibly for other functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.