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Taking a good look at free radicals in the aging process
Open accessAbstract
The mitochondrial free radical theory of aging (MFRTA) proposes that aging is caused by damage to macromolecules by mitochondrial reactive oxygen species (ROS). This is based on the observed association of the rate of aging and the aged phenotype with the generation of ROS and oxidative damage. However, recent findings, in particular in Caenorhabditis elegans but also in rodents, suggest that ROS generation is not the primary or initial cause of aging. Here, we propose that ROS are tightly associated with aging because they play a role in mediating a stress response to age-dependent damage. This could generate the observed correlation between aging and ROS without implying that ROS damage is the earliest trigger or main cause of aging.
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“As chronological age advances, the levels of ROS increase in an attempt to maintain survival until they betray their original purpose and eventually aggravate, rather than alleviate, the age-associated damage”
From The Hallmarks of Aging (2013) · cites this paper as Hekimi et al., 2011
In the citing paper
“In this theory, high levels of ROS promote mtDNA damage and the aged phenotype, while low levels of ROS are signaling molecules that regulate stress response pathways and activate cellular processes that enhance lifespan (Hekimi et al., 2011).”
From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Hekimi et al., 2011
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Metadata
- Authors
- Hekimi, S., Lapointe, J., & Wen, Y.
- Affiliations
- McGill University (CA)
- Corresponding author
- Hekimi, Siegfried
- Venue
- Trends in Cell Biology
- Publisher
- Elsevier BV
- Published
- 2011-10
- Volume
- 21
- Issue
- 10
- Pages
- 569-576
- ISSN
- 0962-8924 (ISSN-L)
- PMC
- PMC4074523
- OpenAlex
- W2085525271
- Cited by
- 606
- References
- 90
- Citations by year
- 2026: 17 · 2025: 19 · 2024: 30 · 2023: 31 · 2022: 45 · 2021: 43 · 2020: 46 · 2019: 43 · 2018: 49 · 2017: 43 · 2016: 51 · 2015: 38 · 2014: 48 · 2013: 57 · 2012: 39
- FWCI
- 5.02
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Trends in Cell Biology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Canadian Institutes of Health Research (97869_1)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Keywords
- reactive oxygen species, aging, oxidative damage, macromolecular damage, stress response, Caenorhabditis elegans, rodents
- MeSH terms
- Aging, Animals, DNA Damage, Free Radicals, Humans, Mitochondria, Models, Molecular, Mutation, Rodentia, Superoxide Dismutase, Signal Transduction, Caenorhabditis elegans, Reactive Oxygen Species, Oxidative Stress
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