The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Oxidative Stress, Accumulation of Biological 'Garbage', and Aging
Abstract
Normal metabolism is associated with unavoidable mild oxidative stress resulting in biomolecular damage that cannot be totally repaired or removed by cellular degradative systems, including lysosomes, proteasomes, and cytosolic and mitochondrial proteases. Consequently, irreversibly damaged and functionally defective structures (biological 'garbage') accumulate within long-lived postmitotic cells, such as cardiac myocytes and neurons, leading to progressive loss of adaptability and increased probability of death and characterizing a process called aging, or senescence. Intralysosomal 'garbage' is represented by lipofuscin (age pigment), an undegradable autophagocytosed material, while extralysosomal 'garbage' involves oxidatively modified cytosolic proteins, altered biomembranes, defective mitochondria and other organelles. In aged postmitotic cells, heavily lipofuscin-loaded lysosomes perform poorly, resulting in the enhanced accumulation of defective mitochondria, which in turn produce more reactive oxygen species causing additional damage (the mitochondrial-lysosomal axis theory). Potential anti-aging strategies may involve not only overall reduction of oxidative stress, but also the use of intralysosomal iron chelators hampering Fenton-type chemistry as well as the stimulation of cellular degradative systems.
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Cites
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Intraneuronal Aβ42 Accumulation in Human Brain
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Mitochondrial DNA mutations in human colonic crypt stem cells
Taylor, R. W., Barron, M. J., Borthwick, G. M., Gospel, A., Chinnery, P. F., Samuels, D. C., Taylor, G. A., Plusa, S. M., Needham, S. J., Greaves, L. C., et al. (2003) · Journal of Clinical Investigation · doi:10.1172/jci19435 · Cited by 530
Cancer and ageing: rival demons?
Campisi, J. (2003) · Nature Reviews Cancer · doi:10.1038/nrc1073 · Cited by 512
Genetic and functional changes in mitochondria associated with aging
Ozawa, T. (1997) · Physiological Reviews · doi:10.1152/physrev.1997.77.2.425 · Cited by 312
Prevention of oxidant-induced cell death by lysosomotropic iron chelators
Persson, H. L., Yu, Z., Tirosh, O., Eaton, J. W., & Brunk, U. T. (2003) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(03)00106-0 · Cited by 185
Self-citationNeurodegeneration in Normal Brain Aging and Disease
Thal, D. R., Del Tredici, K., & Braak, H. (2004) · Science of Aging Knowledge Environment · doi:10.1126/sageke.2004.23.pe26 · Cited by 149
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Achieving the Balance between ROS and Antioxidants: When to Use the Synthetic Antioxidants
Poljsak, B., Šuput, D., & Milisav, I. (2013) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2013/956792 · Cited by 1,301
Mitochondrial dysfunction is a trigger of Alzheimer's disease pathophysiology
Moreira, P. I., Carvalho, C., Zhu, X., Smith, M. A., & Perry, G. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2009.10.006 · Cited by 734
Autophagy failure in Alzheimer's disease—locating the primary defect
Nixon, R. A., & Yang, D.-S. (2011) · Neurobiology of Disease · doi:10.1016/j.nbd.2011.01.021 · Cited by 595
Kell, D. B. (2009) · BMC Medical Genomics · doi:10.1186/1755-8794-2-2 · Cited by 554
Terman, A., Kurz, T., Navratil, M., Arriaga, E. A., & Brunk, U. T. (2010) · Antioxidants & Redox Signaling · doi:10.1089/ars.2009.2598 · Cited by 490
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Metadata
- Authors
- Terman, A., & Brunk, U. T.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2006-01
- Volume
- 8
- Issue
- 1-2
- Pages
- 197-204
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W1982900915
- Cited by
- 363
- References
- 7
- FWCI
- 20.81
- Type
- journal article
- Language
- en
- Open access
- closed
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