The DOI matches its Crossref record; 107 of the 107 references it cites were found in a registry or an index.
Mitochondria, Oxidants, and Aging
Open accessAbstract
The free radical theory of aging postulates that the production of intracellular reactive oxygen species is the major determinant of life span. Numerous cell culture, invertebrate, and mammalian models exist that lend support to this half-century-old hypothesis. Here we review the evidence that both supports and conflicts with the free radical theory and examine the growing link between mitochondrial metabolism, oxidant formation, and the biology of aging.
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In the citing paper
“Mounting evidence has shown that aging is accompanied with the increase of oxidative- stress and inflammation in the brain (Franceschi et al. 2000, Finkel & Holbrook 2000, Balaban et al. 2005, Lee et al. 2000, Guest et al. 2014, Lynch 2010).”
From miR‐186 is decreased in aged brain and suppresses BACE 1 expression (2016) · cites this paper as Balaban et al. 2005
In the citing paper
“Aging is broadly defined by a progressive decline in physiological functions, accompanied with increase of oxidative stress and inflammation in the brain (Franceschi et al. 2000, Finkel & Holbrook 2000, Balaban et al. 2005, Lee et al. 2000, Guest et al. 2014, Lynch 2010, Lopez-Otin et al. 2013).”
From miR‐186 is decreased in aged brain and suppresses BACE 1 expression (2016) · cites this paper as Balaban et al. 2005
In the citing paper
“Mitochondria are a physiologically significant source of ROS with important implications in physiology, not only in cardiovascular disease but in many other conditions like aging (57, 84, 136, 165, 170, 290, 864, 997).”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [57]
In the citing paper
“In brief, longer-lived species generally show higher cellular oxidative stress resistance and lower levels of mitochondrial ROS production than shorter-lived species.”
From DNA Repair, Genome Stability, and Aging (2005) · cites this paper as Balaban et al., 2005
Citations
Cites
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Measuring Mitochondrial Protein Thiol Redox State
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Loss of Fis1 impairs proteostasis during skeletal muscle aging in Drosophila
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A Redox-Switchable Colorimetric Probe for “Naked-Eye” Detection of Hypochlorous Acid and Glutathione
Han, Q., Zhou, F., Wang, Y., Feng, H., Meng, Q., Zhang, Z., & Zhang, R. (2019) · Molecules · doi:10.3390/molecules24132455 · Cited by 23
García‐Matas, S., Paul, R. K., Molina‐Martínez, P., Palacios, H., Gutierrez, V. M., Corpas, R., Pallas, M., Cristòfol, R., de Cabo, R., & Sanfeliu, C. (2015) · Aging Cell · doi:10.1111/acel.12259 · Cited by 22
Advancements in MAFLD Modeling with Human Cell and Organoid Models
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“During the aging process, factors such as accumulated reactive oxygen species (ROS), DNA damage, and impaired mitophagy can lead to mitochondrial dysfunction (Balaban et al, 2005; Linnane et al, 1989; Wallace, 1992).”
Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease?
Hindle, A., Singh, S. P., Pradeepkiran, J. A., Bose, C., Vijayan, M., Kshirsagar, S., Sawant, N. A., & Reddy, P. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116098 · Cited by 14
Potential Role for Herpesviruses in Alzheimer’s Disease
Duggan, M. R., Torkzaban, B., Ahooyi, T. M., & Khalili, K. (2020) · Journal of Alzheimer's Disease · doi:10.3233/jad-200814 · Cited by 13
Molecular Perspectives of Mitochondrial Adaptations and Their Role in Cardiac Proteostasis
Alam, S., Abdullah, C. S., Aishwarya, R., Morshed, M., & Bhuiyan, M. S. (2020) · Frontiers in Physiology · doi:10.3389/fphys.2020.01054 · Cited by 12
Mitochondrial Function and Neurodegenerative Diseases
Wilkins, H. M., Weidling, I., Koppel, S., Wang, X., von Schulze, A., & Swerdlow, R. H. (2018) · The Molecular and Cellular Basis of Neurodegenerative Diseases · doi:10.1016/b978-0-12-811304-2.00013-4 · Cited by 2
Li, Z., Hu, S., Liu, Z., Zhang, M., Chen, S., Yu, W., Ding, M., Fan, Y., Li, S., & Jin, J. (2026) · International Journal of Biological Sciences · doi:10.7150/ijbs.130242
Metadata
- Authors
- Balaban, R. S., Nemoto, S., & Finkel, T.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Finkel, Toren
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2005-02
- Volume
- 120
- Issue
- 4
- Pages
- 483-495
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2121966499
- Cited by
- 4,388
- References
- 107
- Citations by year
- 2026: 119 · 2025: 172 · 2024: 217 · 2023: 247 · 2022: 250 · 2021: 285 · 2020: 243 · 2019: 203 · 2018: 230 · 2017: 214 · 2016: 221 · 2015: 241 · 2014: 245 · 2013: 220 · 2012: 213
- FWCI
- 11.51
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- 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
- free radical theory of aging, reactive oxygen species, mitochondria, mitochondrial metabolism, oxidizing agents, aging, lifespan, oxidative stress
- MeSH terms
- Aging, Animals, Free Radicals, Mitochondria, Mutation, Nutritional Physiological Phenomena, Yeasts, Oxidants, Reactive Oxygen Species
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