The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Autophagy, organelles and ageing
Abstract
As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy and other degradative systems, long‐lived postmitotic cells, such as cardiac myocytes, neurons and retinal pigment epithelial cells, progressively accumulate biological ‘garbage’ (‘waste’ materials). The latter include lipofuscin (a non‐degradable intralysosomal polymeric substance), defective mitochondria and other organelles, and aberrant proteins, often forming aggregates (aggresomes). An interaction between senescent lipofuscin‐loaded lysosomes and mitochondria seems to play a pivotal role in the progress of cellular ageing. Lipofuscin deposition hampers autophagic mitochondrial turnover, promoting the accumulation of senescent mitochondria, which are deficient in ATP production but produce increased amounts of reactive oxygen species. Increased oxidative stress, in turn, further enhances damage to both mitochondria and lysosomes, thus diminishing adaptability, triggering mitochondrial and lysosomal pro‐apoptotic pathways, and culminating in cell death. Copyright © 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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Cites
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
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Free Radicals in Biology and Medicine
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Macroautophagy—a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease
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Self-citationMitochondrial 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
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Genetic and functional changes in mitochondria associated with aging
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Cited by
Necroptosis, necrosis and secondary necrosis converge on similar cellular disintegration features
Berghe, T. V., Vanlangenakker, N., Parthoens, E., Deckers, W., Devos, M., Festjens, N., Guerin, C. J., Brunk, U. T., Declercq, W., & Vandenabeele, P. (2010) · Cell Death & Differentiation · doi:10.1038/cdd.2009.184 · Cited by 639
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Self-citationLipofuscin: Formation, Distribution, and Metabolic Consequences
JUNG, T., BADER, N., & GRUNE, T. (2007) · Annals of the New York Academy of Sciences · doi:10.1196/annals.1404.008 · Cited by 415
Neurodegenerative lysosomal disorders: A continuum from development to late age
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Aging and Immune Function: Molecular Mechanisms to Interventions
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Metadata
- Authors
- Terman, A., Gustafsson, B., & Brunk, U.
- Venue
- The Journal of Pathology
- Publisher
- Wiley
- Published
- 2007-01
- Volume
- 211
- Issue
- 2
- Pages
- 134-143
- ISSN
- 0022-3417 (ISSN-L)
- 1096-9896
- OpenAlex
- W1989899139
- Cited by
- 285
- References
- 9
- FWCI
- 20.94
- Type
- journal article
- Language
- en
- Open access
- closed
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