The DOI matches its Crossref record; 128 of the 129 references it cites were found in a registry or an index.
Lysosomes and oxidative stress in aging and apoptosis
Abstract
The lysosomal compartment consists of numerous acidic vesicles (pH approximately 4-5) that constantly fuse and divide. It receives a large number of hydrolases from the trans-Golgi network, while their substrates arrive from both the cell's outside (heterophagy) and inside (autophagy). Many macromolecules under degradation inside lysosomes contain iron that, when released in labile form, makes lysosomes sensitive to oxidative stress. The magnitude of generated lysosomal destabilization determines if reparative autophagy, apoptosis, or necrosis will follow. Apart from being an essential turnover process, autophagy is also a mechanism for cells to repair inflicted damage, and to survive temporary starvation. The inevitable diffusion of hydrogen peroxide into iron-rich lysosomes causes the slow oxidative formation of lipofuscin in long-lived postmitotic cells, where it finally occupies a substantial part of the volume of the lysosomal compartment. This seems to result in a misdirection of lysosomal enzymes away from autophagosomes, resulting in depressed autophagy and the accumulation of malfunctioning mitochondria and proteins with consequent cellular dysfunction. This scenario might put aging into the category of autophagy disorders.
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“ROS play a prominent causal role in LMP, not only as the H2O2-driven luminal production of hydroxyl radicals by Fenton reactions destabilizes the lysosomal membrane upon lipid peroxidation [766, 767]”
From Molecular mechanisms of cell death: recommendations of the nomenclature committee on cell death 2018. (2018) · cites this paper as [766]
In the citing paper
“Moreover, damaged mitochondria are insensitive to mitophagy (i.e., selective autophagy of mitochondria), and consequently, mitochondrial number and size are not properly regulated in senescent cells [214].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [214]
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1 retracted
Chen, W., Li, N., Chen, T., Han, Y., Li, C., Wang, Y., He, W., Zhang, L., Wan, T. Y., & Cao, X. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m502190200 · Cited by 82
RetractedThe 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
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
Self-eating and self-killing: crosstalk between autophagy and apoptosis
Maiuri, M. C., Zalckvar, E., Kimchi, A., & Kroemer, G. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2239 · Cited by 3,638
de Duve, C., & Wattiaux, R. (1966) · Annual Review of Physiology · doi:10.1146/annurev.ph.28.030166.002251 · Cited by 3,033
Autophagy in Health and Disease: A Double-Edged Sword
Shintani, T., & Klionsky, D. J. (2004) · Science · doi:10.1126/science.1099993 · Cited by 2,559
Ohkuma, S., & Poole, B. (1978) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.75.7.3327 · Cited by 2,173
Autophagy: from phenomenology to molecular understanding in less than a decade
Klionsky, D. J. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2245 · Cited by 1,977
Lysosomes: fusion and function
Luzio, J. P., Pryor, P. R., & Bright, N. A. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2217 · Cited by 1,807
Autophagy: molecular machinery for self-eating
Yorimitsu, T., & Klionsky, D. J. (2005) · Cell Death and Differentiation · doi:10.1038/sj.cdd.4401765 · Cited by 1,572
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Protein oxidation and peroxidation
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Metadata
- Authors
- Kurz, T., Terman, A., Gustafsson, B., & Brunk, U. T.
- Affiliations
- Linköping University (SE)
- Linköping University Hospital (SE)
- Corresponding author
- Brunk, Ulf T.
- Venue
- Biochimica et Biophysica Acta (BBA) - General Subjects
- Publisher
- Elsevier BV
- Published
- 2008-11
- Volume
- 1780
- Issue
- 11
- Pages
- 1291-1303
- ISSN
- 0304-4165 (ISSN-L)
- OpenAlex
- W2056367295
- Cited by
- 287
- References
- 129
- Citations by year
- 2026: 13 · 2025: 11 · 2024: 9 · 2023: 7 · 2022: 13 · 2021: 14 · 2020: 14 · 2019: 21 · 2018: 13 · 2017: 13 · 2016: 21 · 2015: 11 · 2014: 23 · 2013: 16 · 2012: 15
- FWCI
- 2.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biochimica et Biophysica Acta (BBA) - General Subjects (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- lysosomes, oxidative stress, aging, apoptosis, autophagy, iron release, lipofuscin, lysosomal destabilization, hydrogen peroxide, mitochondrial dysfunction, lysosomal enzymes, necrosis, starvation survival
- MeSH terms
- Aging, Animals, Humans, Iron, Lysosomes, Mitosis, Apoptosis, Oxidative Stress
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