The DOI matches its Crossref record; 142 of the 143 references it cites were found in a registry or an index.
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
In the citing paper
“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
In the citing paper
“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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Cites
2 retracted
Wenz, T., Rossi, S. G., Rotundo, R. L., Spiegelman, B. M., & Moraes, C. T. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911570106 · Cited by 600
RetractedSafdar, A., Bourgeois, J. M., Ogborn, D. I., Little, J. P., Hettinga, B. P., Akhtar, M., Thompson, J. E., Melov, S., Mocellin, N. J., Kujoth, G. C., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1019581108 · Cited by 320
RetractedLópez-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Aging: a theory based on free radical and radiation chemistry
Harman, D. (1956) · Journal of Gerontology · doi:10.1093/geronj/11.3.298 · Cited by 8,567
Inflamm‐aging: An Evolutionary Perspective on Immunosenescence
FRANCESCHI, C., BONAFÈ, M., VALENSIN, S., OLIVIERI, F., DE LUCA, M., OTTAVIANI, E., & DE BENEDICTIS, G. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb06651.x · Cited by 5,358
Pleiotropy, natural selection, and the evolution of senescence.
Williams, G. C. (1957) · Evolution · doi:10.1111/j.1558-5646.1957.tb02911.x · Cited by 4,279
Circulating mitochondrial DAMPs cause inflammatory responses to injury
Zhang, Q., Raoof, M., Chen, Y., Sumi, Y., Sursal, T., Junger, W., Brohi, K., Itagaki, K., & Hauser, C. J. (2010) · Nature · doi:10.1038/nature08780 · Cited by 3,812
Seth, R. B., Sun, L., Ea, C.-K., & Chen, Z. J. (2005) · Cell · doi:10.1016/j.cell.2005.08.012 · Cited by 3,329
Goodpaster, B. H., Park, S. W., Harris, T. B., Kritchevsky, S. B., Nevitt, M., Schwartz, A. V., Simonsick, E. M., Tylavsky, F. A., Visser, M., Newman, A. B., et al. (2006) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/61.10.1059 · Cited by 3,083
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Twig, G., Elorza, A., Molina, A. J. A., Mohamed, H., Wikstrom, J. D., Walzer, G., Stiles, L., Haigh, S. E., Katz, S., Las, G., et al. (2008) · The EMBO Journal · doi:10.1038/sj.emboj.7601963 · Cited by 3,082
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Sorted by citations
Aging and aging-related diseases: from molecular mechanisms to interventions and treatments
Guo, J., Huang, X., Dou, L., Yan, M., Shen, T., Tang, W., & Li, J. (2022) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-022-01251-0 · Cited by 1,976
From discoveries in ageing research to therapeutics for healthy ageing
Campisi, J., Kapahi, P., Lithgow, G. J., Melov, S., Newman, J. C., & Verdin, E. (2019) · Nature · doi:10.1038/s41586-019-1365-2 · Cited by 1,389
Age and Age-Related Diseases: Role of Inflammation Triggers and Cytokines
Rea, I. M., Gibson, D. S., McGilligan, V., McNerlan, S. E., Alexander, H. D., & Ross, O. A. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00586 · Cited by 1,267
Senescence and aging: Causes, consequences, and therapeutic avenues
McHugh, D., & Gil, J. (2018) · Journal of Cell Biology · doi:10.1083/jcb.201708092 · Cited by 1,233
Redox metabolism: ROS as specific molecular regulators of cell signaling and function
Lennicke, C., & Cochemé, H. M. (2021) · Molecular Cell · doi:10.1016/j.molcel.2021.08.018 · Cited by 1,313
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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