ArticleGeroScience2020
Mitochondrial base excision repair positively correlates with longevity in the liver and heart of mammals.
Article in GeroScience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- Genetic associations with longevity in a Calabrian cohort: an exploratory genome-wide study.GeroScience · 2026Article
- ROS-Mediated Cardiomyocyte Proliferation and Myocardial Regeneration: Mechanisms and Targeted Strategies for Ischemic Heart Disease.Journal of cardiovascular development and disease · 2026Review
- Unlocking longevity through the comparative biology of aging.Nature aging · 2025Review
- The impact of oxidative stress-induced mitochondrial dysfunction on diabetic microvascular complications.Frontiers in endocrinology · 2023Review
- Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- The landscape of aging.Science China. Life sciences · 2022Review
- Vegetables and Their Bioactive Compounds as Anti-Aging Drugs.Molecules (Basel, Switzerland) · 2022Review
- Role of the mtDNA Mutations and Mitophagy in Inflammaging.International journal of molecular sciences · 2022Review
- Article
- Alginate oligosaccharide alleviates D-galactose-induced cardiac ageing via regulating myocardial mitochondria function and integrity in mice.Journal of cellular and molecular medicine · 2021Article
- Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Damage to DNA is especially important for aging. High DNA repair could contribute, in principle, to lower such damage in long-lived species. However, previous studies showed that repair of endogenous damage to nuclear DNA (base excision repair, BER) is negatively or not correlated with mammalian longevity. However, we hypothesize here that mitochondrial, instead of nuclear, BER is higher in long-lived than in short-lived mammals. We have thus measured activities and/or protein levels of various BER enzymes including DNA glycosylases, NTHL1 and NEIL2, and the APE endonuclease both in total and mitochondrial liver and heart fractions from up to eight mammalian species differing by 13-fold in longevity. Our results show, for the first time, a positive correlation between (mitochondrial) BER and mammalian longevity. This suggests that the low steady-state oxidative damage in mitochondrial DNA of long-lived species would be due to both their lower mitochondrial ROS generation and their higher mitochondrial BER. Long-lived mammals do not need to continuously maintain high nuclear BER levels because they release less mitROS to the cytosol. This can be the reason why they tend to show lower nuclear BER values. The higher mitochondrial BER of long-lived mammals contributes to their superior longevity, agrees with the updated version of the mitochondrial free radical theory of aging, and indicates the special relevance of mitochondria and mitROS for aging.
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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.