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The Mitochondrial Basis of Aging
Open accessAbstract
A decline in mitochondrial quality and activity has been associated with normal aging and correlated with the development of a wide range of age-related diseases. Here, we review the evidence that a decline in mitochondria function contributes to aging. In particular, we discuss how mitochondria contribute to specific aspects of the aging process, including cellular senescence, chronic inflammation, and the age-dependent decline in stem cell activity. Signaling pathways regulating the mitochondrial unfolded protein response and mitophagy are also reviewed, with particular emphasis placed on how these pathways might, in turn, regulate longevity. Taken together, these observations suggest that mitochondria influence or regulate a number of key aspects of aging and suggest that strategies directed at improving mitochondrial quality and function might have far-reaching beneficial effects.
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“There is longstanding evidence that the decline in mitochondrial function with aging, may contribute to age-associated dysregulation in energy homeostasis and increased predisposition to age-related diseases”
From Benefits of Metformin in Attenuating the Hallmarks of Aging (2020) · cites this paper as Sun et al. 2016
In the citing paper
“For example, in yeast and animals, mitochondrial dysfunction increases with age and may contribute to the progression of aging (Sun et al., 2016).”
From The Aging Epigenome (2016) · cites this paper as Sun et al., 2016
In the citing paper
“mutations in mtDNA, and changes inmitochondrial biogenesis have been functionally implicated in the progression of aging (reviewed by Sun et al., 2016).”
From The Aging Epigenome (2016) · cites this paper as Sun et al., 2016
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“As cells age, mitochondrial turnover declines and mitochondrial dysfunction increases (Sun et al., 2016).”
From The Aging Epigenome (2016) · cites this paper as Sun et al., 2016
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“changes in the activity of the transcription activator PGC-1α with age contribute to the loss of mitochondrial biogenesis and function (Rera et al., 2011; Sun et al., 2016).”
From The Aging Epigenome (2016) · cites this paper as Sun et al., 2016
In the citing paper
“In addition to inducing protection of nuclear DNA from oxidative damage, mROS initiate signals that activate several pathways that protect mitochondria from oxidative stress. These pathways slow aging, inhibit cell death and may result in lifespan extension [67,108,109].”
From The mitochondrial permeability transition: Nexus of aging, disease and longevity (2021) · cites this paper as [67]
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Self-citation
Metadata
- Authors
- Sun, N., Youle, R. J., & Finkel, T.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Youle, Richard J.
- Finkel, Toren
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2016-03
- Volume
- 61
- Issue
- 5
- Pages
- 654-666
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC4779179
- OpenAlex
- W2289876562
- Cited by
- 1,441
- References
- 143
- Citations by year
- 2026: 162 · 2025: 151 · 2024: 148 · 2023: 158 · 2022: 165 · 2021: 189 · 2020: 168 · 2019: 110 · 2018: 95 · 2017: 63 · 2016: 30
- FWCI
- 8.97
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Soochow University
- National Institutes of Health
- National Heart, Lung, and Blood Institute (ZIAHL005012)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial dysfunction, aging, cellular senescence, chronic inflammation, stem cell aging, mitochondrial unfolded protein response, mitophagy, longevity, age-related diseases, mitochondrial quality
- MeSH terms
- Age Factors, Aging, Animals, Humans, Inflammation, Longevity, Mitochondria, Stem Cells, Signal Transduction, Cellular Senescence, Unfolded Protein Response, Mitophagy
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