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Oxidative Stress, Mitochondrial Dysfunction, and Aging
Open accessAbstract
Aging is an intricate phenomenon characterized by progressive decline in physiological functions and increase in mortality that is often accompanied by many pathological diseases. Although aging is almost universally conserved among all organisms, the underlying molecular mechanisms of aging remain largely elusive. Many theories of aging have been proposed, including the free-radical and mitochondrial theories of aging. Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA. In this paper, we will present the current understanding of the interplay between ROS and mitochondria and will discuss their potential impact on aging and age-related diseases.
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Citations
Cites
The serial cultivation of human diploid cell strains
Hayflick, L., & Moorhead, P. S. (1961) · Experimental Cell Research · doi:10.1016/0014-4827(61)90192-6 · Cited by 8,508
MACDONALD, M. (1993) · Cell · doi:10.1016/0092-8674(93)90585-e · Cited by 8,366
Mitochondrial Dysfunction and Oxidative Stress in Neurodegenerative Diseases
Lin, M. T., & Beal, M. F. (2006) · Nature · doi:10.1038/nature05292 · Cited by 6,455
Mitochondrial formation of reactive oxygen species
Turrens, J. F. (2003) · The Journal of Physiology · doi:10.1113/jphysiol.2003.049478 · Cited by 5,084
Extension of Life-Span by Introduction of Telomerase into Normal Human Cells
Bodnar, A. G., Ouellette, M., Frolkis, M., Holt, S. E., Chiu, C.-P., Morin, G. B., Harley, C. B., Shay, J. W., Lichtsteiner, S., & Wright, W. E. (1998) · Science · doi:10.1126/science.279.5349.349 · Cited by 4,975
Parkin is recruited selectively to impaired mitochondria and promotes their autophagy
Narendra, D., Tanaka, A., Suen, D.-F., & Youle, R. J. (2008) · The Journal of Cell Biology · doi:10.1083/jcb.200809125 · Cited by 4,026
Hereditary Early-Onset Parkinson's Disease Caused by Mutations in PINK1
Valente, E. M., Abou-Sleiman, P. M., Caputo, V., Muqit, M. M. K., Harvey, K., Gispert, S., Ali, Z., Del Turco, D., Bentivoglio, A. R., Healy, D. G., et al. (2004) · Science · doi:10.1126/science.1096284 · Cited by 3,481
Oxidative DNA damage: mechanisms, mutation, and disease
Cooke, M. S., Evans, M. D., Dizdaroglu, M., & Lunec, J. (2003) · The FASEB Journal · doi:10.1096/fj.02-0752rev · Cited by 3,245
NOX enzymes and the biology of reactive oxygen
Lambeth, J. D. (2004) · Nature Reviews Immunology · doi:10.1038/nri1312 · Cited by 3,125
Premature ageing in mice expressing defective mitochondrial DNA polymerase
Trifunovic, A., Wredenberg, A., Falkenberg, M., Spelbrink, J. N., Rovio, A. T., Bruder, C. E., Bohlooly-Y, M., Gidlöf, S., Oldfors, A., Wibom, R., et al. (2004) · Nature · doi:10.1038/nature02517 · Cited by 2,734
Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors
Campisi, J. (2005) · Cell · doi:10.1016/j.cell.2005.02.003 · Cited by 2,379 · cited 1×
“Because mitochondria are the major producer of ROS in mammalian cells, the close proximity to ROS places mitochondrial DNA (mtDNA) prone to oxidative damage [104].”
BackgroundRavikumar, B., Vacher, C., Berger, Z., Davies, J. E., Luo, S., Oroz, L. G., Scaravilli, F., Easton, D. F., Duden, R., O'Kane, C. J., et al. (2004) · Nature Genetics · doi:10.1038/ng1362 · Cited by 2,347
Bjelakovic, G., Nikolova, D., Gluud, L. L., Simonetti, R. G., & Gluud, C. (2007) · JAMA · doi:10.1001/jama.297.8.842 · Cited by 2,275
Mitochondrial DNA mutations, oxidative stress, and apoptosis in mammalian aging
Kujoth, G. C., Hiona, A., Pugh, T. D., Someya, S., Panzer, K., Wohlgemuth, S. E., Hofer, T., Seo, A. Y., Sullivan, R., Jobling, W. A., et al. (2005) · Science · doi:10.1126/science.1112125 · Cited by 2,165
Understanding the odd science of aging
Kirkwood, T. B. L. (2005) · Cell · doi:10.1016/j.cell.2005.01.027 · Cited by 1,984
Toxic Metals and Oxidative Stress Part I: Mechanisms Involved in Me-tal induced Oxidative Damage
Nuran Ercal, B. S. P., Hande Gurer-Orhan, B. S. P., & Nukhet Aykin-Burns, B. S. P. (2001) · Current Topics in Medicinal Chemistry · doi:10.2174/1568026013394831 · Cited by 1,944
Dilated cardiomyopathy and neonatal lethality in mutant mice lacking manganese superoxide dismutase
Li, Y., Huang, T.-T., Carlson, E. J., Melov, S., Ursell, P. C., Olson, J. L., Noble, L. J., Yoshimura, M. P., Berger, C., Chan, P. H., et al. (1995) · Nature Genetics · doi:10.1038/ng1295-376 · Cited by 1,789
Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin
Clark, I. E., Dodson, M. W., Jiang, C., Cao, J. H., Huh, J. R., Seol, J. H., Yoo, S. J., Hay, B. A., & Guo, M. (2006) · Nature · doi:10.1038/nature04779 · Cited by 1,788
Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin
Park, J., Lee, S. B., Lee, S., Kim, Y., Song, S., Kim, S., Bae, E., Kim, J., Shong, M., Kim, J.-M., et al. (2006) · Nature · doi:10.1038/nature04788 · Cited by 1,705
Hussain, S. P., Hofseth, L. J., & Harris, C. C. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1046 · Cited by 1,690 · cited 1×
“hyperoxia, toxins, and transition metals [16–26].”
FoxOs Are Critical Mediators of Hematopoietic Stem Cell Resistance to Physiologic Oxidative Stress
Tothova, Z., Kollipara, R., Huntly, B. J., Lee, B. H., Castrillon, D. H., Cullen, D. E., McDowell, E. P., Lazo-Kallanian, S., Williams, I. R., Sears, C., et al. (2007) · Cell · doi:10.1016/j.cell.2007.01.003 · Cited by 1,562
α-Synuclein Is Degraded by Both Autophagy and the Proteasome
Webb, J. L., Ravikumar, B., Atkins, J., Skepper, J. N., & Rubinsztein, D. C. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m300227200 · Cited by 1,429
Oxidative DNA damage and disease: induction, repair and significance
Evans, M. D., Dizdaroglu, M., & Cooke, M. S. (2004) · Mutation Research/Reviews in Mutation Research · doi:10.1016/j.mrrev.2003.11.001 · Cited by 1,372
The sites and topology of mitochondrial superoxide production
Brand, M. D. (2010) · Experimental Gerontology · doi:10.1016/j.exger.2010.01.003 · Cited by 1,217
Regulation of oxidative stress by ATM is required for self-renewal of haematopoietic stem cells
Ito, K., Hirao, A., Arai, F., Matsuoka, S., Takubo, K., Hamaguchi, I., Nomiyama, K., Hosokawa, K., Sakurada, K., Nakagata, N., et al. (2004) · Nature · doi:10.1038/nature02989 · Cited by 1,175 · cited 2×
“Deletion of Ataxia telangiectasia mutated (ATM) kinase results in increased ROS level in hematopoietic stem cell (HSC) population in aged mice, which correlates with a rapid decline in HSC number and function [95].”
BackgroundCell intrinsic alterations underlie hematopoietic stem cell aging
Rossi, D. J., Bryder, D., Zahn, J. M., Ahlenius, H., Sonu, R., Wagers, A. J., & Weissman, I. L. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0503280102 · Cited by 1,152 · cited 2×
“Particularly, mitochondria are thought to play an important role in the pathogenesis of age-associated neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and Huntington’s disease.”
BackgroundDeficiencies in DNA damage repair limit the function of haematopoietic stem cells with age
Rossi, D. J., Bryder, D., Seita, J., Nussenzweig, A., Hoeijmakers, J., & Weissman, I. L. (2007) · Nature · doi:10.1038/nature05862 · Cited by 1,115
Early mitochondrial calcium defects in Huntington's disease are a direct effect of polyglutamines
Panov, A. V., Gutekunst, C.-A., Leavitt, B. R., Hayden, M. R., Burke, J. R., Strittmatter, W. J., & Greenamyre, J. T. (2002) · Nature Neuroscience · doi:10.1038/nn884 · Cited by 1,030
Weisiger, R. A., & Fridovich, I. (1973) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(19)43969-0 · Cited by 895
Mitochondrial DNA deletions in human brain: regional variability and increase with advanced age
Corral-Debrinski, M., Horton, T., Lott, M. T., Shoffner, J. M., Flint Beal, M., & Wallace, D. C. (1992) · Nature Genetics · doi:10.1038/ng1292-324 · Cited by 890
Mutagenesis by 8-oxoguanine: an enemy within
Grollman, A. P., & Moriya, M. (1993) · Trends in Genetics · doi:10.1016/0168-9525(93)90089-z · Cited by 807
Yang, Y., Gehrke, S., Imai, Y., Huang, Z., Ouyang, Y., Wang, J.-W., Yang, L., Beal, M. F., Vogel, H., & Lu, B. (2006) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0602493103 · Cited by 798
Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence
Passos, J. F., Saretzki, G., Ahmed, S., Nelson, G., Richter, T., Peters, H., Wappler, I., Birket, M. J., Harold, G., Schaeuble, K., et al. (2007) · PLoS Biology · doi:10.1371/journal.pbio.0050110 · Cited by 796
Does oxidative damage to DNA increase with age?
Hamilton, M. L., Van Remmen, H., Drake, J. A., Yang, H., Guo, Z. M., Kewitt, K., Walter, C. A., & Richardson, A. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.171202698 · Cited by 768
Oxidative damage to mitochondrial DNA shows marked age-dependent increases in human brain
Mecocci, P., MacGarvey, U., Kaufman, A. E., Koontz, D., Shoffner, J. M., Wallace, D. C., & Beal, M. F. (1993) · Annals of Neurology · doi:10.1002/ana.410340416 · Cited by 757
Van Remmen, H., Ikeno, Y., Hamilton, M., Pahlavani, M., Wolf, N., Thorpe, S. R., Alderson, N. L., Baynes, J. W., Epstein, C. J., Huang, T.-T., et al. (2003) · Physiological Genomics · doi:10.1152/physiolgenomics.00122.2003 · Cited by 734
Oxidative DNA damage and senescence of human diploid fibroblast cells.
Chen, Q., Fischer, A., Reagan, J. D., Yan, L. J., & Ames, B. N. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.10.4337 · Cited by 720
Elchuri, S., Oberley, T. D., Qi, W., Eisenstein, R. S., Jackson Roberts, L., Van Remmen, H., Epstein, C. J., & Huang, T.-T. (2005) · Oncogene · doi:10.1038/sj.onc.1208207 · Cited by 667
Endurance Exercise as a Countermeasure for Aging
Lanza, I. R., Short, D. K., Short, K. R., Raghavakaimal, S., Basu, R., Joyner, M. J., McConnell, J. P., & Nair, K. S. (2008) · Diabetes · doi:10.2337/db08-0349 · Cited by 582
Dependence of H2O2 formation by rat heart mitochondria on substrate availability and donor age
Hansford, R. G., Hogue, B. A., & Mildaziene, V. (1997) · Journal of Bioenergetics and Biomembranes · doi:10.1023/a:1022420007908 · Cited by 447 · cited 1×
“Mitochondria are the major producer of ROS in cells, and the bulk of mitochondrial ROS is generated at the electron transport chain [5, 6].”
BackgroundControl of the replicative life span of human fibroblasts by p16 and the polycomb protein Bmi-1
Itahana, K., Zou, Y., Itahana, Y., Martinez, J.-L., Beausejour, C., Jacobs, J. J. L., van Lohuizen, M., Band, V., Campisi, J., & Dimri, G. P. (2003) · Molecular and Cellular Biology · doi:10.1128/mcb.23.1.389-401.2003 · Cited by 438
Barazzoni, R., Short, K. R., & Nair, K. S. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.275.5.3343 · Cited by 367
Xie, Y., Yang, H., Cunanan, C., Okamoto, K., Shibata, D., Pan, J., Barnes, D. E., Lindahl, T., McIlhatton, M., Fishel, R., et al. (2004) · Cancer Research · doi:10.1158/0008-5472.can-03-3834 · Cited by 291
Oxidative damage in telomeric DNA disrupts recognition by TRF1 and TRF2
Opresko, P. L. (2005) · Nucleic Acids Research · doi:10.1093/nar/gki273 · Cited by 289
Cytochrome c oxidase is decreased in Alzheimer’s disease platelets
Cardoso, S. M., Proença, M. T., Santos, S., Santana, I., & Oliveira, C. R. (2004) · Neurobiology of Aging · doi:10.1016/s0197-4580(03)00033-2 · Cited by 281
Serra, V., von Zglinicki, T., Lorenz, M., & Saretzki, G. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m207939200 · Cited by 278
Yalcin, S., Zhang, X., Luciano, J. P., Mungamuri, S. K., Marinkovic, D., Vercherat, C., Sarkar, A., Grisotto, M., Taneja, R., & Ghaffari, S. (2008) · Journal of Biological Chemistry · doi:10.1074/jbc.m800517200 · Cited by 247
Ubiquitous overexpression of CuZn superoxide dismutase does not extendlife span in mice
(2000) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/55.1.b5 · Cited by 216
Reduction in glutathione peroxidase 4 increases life span through increased sensitivity to apoptosis
Ran, Q., Liang, H., Ikeno, Y., Qi, W., Prolla, T. A., Roberts, L. J., Wolf, N., VanRemmen, H., & Richardson, A. (2007) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/62.9.932 · Cited by 195
Cellular effects of long wavelength UV light (UVA) in mammalian cells
McMillan, T. J., Leatherman, E., Ridley, A., Shorrocks, J., Tobi, S. E., & Whiteside, J. R. (2008) · Journal of Pharmacy and Pharmacology · doi:10.1211/jpp.60.8.0004 · Cited by 146
Sohal, R. S., Kamzalov, S., Sumien, N., Ferguson, M., Rebrin, I., Heinrich, K. R., & Forster, M. J. (2006) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2005.08.037 · Cited by 131
Reduced amount of mitochondrial DNA in aged human muscle
Welle, S., Bhatt, K., Shah, B., Needler, N., Delehanty, J. M., & Thornton, C. A. (2003) · Journal of Applied Physiology · doi:10.1152/japplphysiol.01061.2002 · Cited by 86
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Ageing, age-related diseases and oxidative stress: What to do next?
Luo, J., Mills, K., le Cessie, S., Noordam, R., & van Heemst, D. (2020) · Ageing Research Reviews · doi:10.1016/j.arr.2019.100982 · Cited by 581
Functional role of mitochondrial respiratory supercomplexes
Genova, M. L., & Lenaz, G. (2014) · Biochimica et Biophysica Acta (BBA) - Bioenergetics · doi:10.1016/j.bbabio.2013.11.002 · Cited by 306
Effects of Glucagon-Like Peptide-1 on Oxidative Stress and Nrf2 Signaling
Oh, Y., & Jun, H.-S. (2017) · International Journal of Molecular Sciences · doi:10.3390/ijms19010026 · Cited by 217
“Many theories on aging have been proposed, and the free-radical theory suggests that cumulative damage to mitochondria and mitochondrial DNA caused by ROS is one of the important causes of aging and aging-related diseases [33].”
BackgroundMaintenance of age in human neurons generated by microRNA-based neuronal conversion of fibroblasts
Huh, C. J., Zhang, B., Victor, M. B., Dahiya, S., Batista, L. F., Horvath, S., & Yoo, A. S. (2016) · eLife · doi:10.7554/elife.18648 · Cited by 213
“reported to increase with age, in part due to the accumulation of reactive oxygen species (ROS) (Keating, 2008; Prigione et al., 2010; Suhr et al., 2010; Cui et al., 2012).”
BackgroundLipid (per) oxidation in mitochondria: an emerging target in the ageing process?
Ademowo, O. S., Dias, H. K. I., Burton, D. G. A., & Griffiths, H. R. (2017) · Biogerontology · doi:10.1007/s10522-017-9710-z · Cited by 184
Metadata
- Authors
- Cui, H., Kong, Y., & Zhang, H.
- Venue
- Journal of Signal Transduction
- Publisher
- Wiley
- Published
- 2012-10-02
- Volume
- 2012
- Pages
- 1-13
- ISSN
- 2090-1739 (ISSN-L)
- 2090-1747
- OpenAlex
- W2021460489
- Cited by
- 1,022
- References
- 52
- FWCI
- 10.23
- Type
- journal article
- Language
- en
- Open access
- hybrid
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