The DOI matches its Crossref record; 245 of the 246 references it cites were found in a registry or an index.
Mitochondrial Dynamics in Aging and Disease
Abstract
Mitochondria are self-replicating organelles but nevertheless strongly depend on supply coded in nuclear genes. They serve many physiological demands in living cells. Supply of the cytoplasm with ATP and engagement in Ca(2+) regulation belong to the main functions of mitochondria. In large eukaryotic cells, in particular in neurons, with their long dendrites and axons, mitochondria have to move to the sites of their action. This trafficking involves several motor molecules and mechanisms to sense the sites of requirements of mitochondria. With aging and as a consequence of some diseases, mitochondrial components may be rendered dysfunctional, and mtDNA mutations arise during the course of replication and by the action of reactive oxygen species. Mutants in motor molecules engaged in trafficking and in the machinery of fusion and fission are causing severe deficiencies on the cellular level; they support neurodegeneration and, thus, cause many diseases. Frequent fusion and fission events mediate the elimination of impaired parts from mitochondria which finally will be degraded by autophagosomes. Extensive fusion provides a basis for functional complementation. Mobility of proteins and small molecules within the mitochondria is necessary to reach the functional goals of fusion and fission, although cristae and a large fraction of proteins of the respiratory complexes proved to be stable for hours after fusion and perform slow exchange of material.
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“As expected, ageing is associated with decreases in both fission and fusion (Bereiter-Hahn, 2014; Chauhan et al., 2014; Jendrach et al., 2005; Seo et al., 2010).”
From Role of the mitochondrial DNA replication machinery in mitochondrial DNA mutagenesis, aging and age-related diseases (2017) · cites this paper as Bereiter-Hahn, 2014
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Cites
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DeBalsi, K. L., Hoff, K. E., & Copeland, W. C. (2017) · Ageing Research Reviews · doi:10.1016/j.arr.2016.04.006 · Cited by 180
Huang, M., Chiang, S., Kalinowski, D. S., Bae, D.-H., Sahni, S., & Richardson, D. R. (2019) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2019/6392763 · Cited by 155
Scheff, S. W., Ansari, M. A., & Mufson, E. J. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.02.030 · Cited by 100
A PGAM5–KEAP1–Nrf2 complex is required for stress-induced mitochondrial retrograde trafficking
O'Mealey, G. B., Plafker, K. S., Berry, W. L., Janknecht, R., Chan, J. Y., & Plafker, S. M. (2017) · Journal of Cell Science · doi:10.1242/jcs.203216 · Cited by 99
Szeto, H. H., & Liu, S. (2018) · Archives of Biochemistry and Biophysics · doi:10.1016/j.abb.2018.10.013 · Cited by 89
Metadata
- Authors
- Bereiter-Hahn, J.
- Venue
- Progress in molecular biology and translational science
- Publisher
- Elsevier
- Published
- 2014
- Volume
- 127
- Pages
- 93-131
- ISSN
- 1877-1173 (ISSN-L)
- OpenAlex
- W2405770350
- Cited by
- 48
- References
- 246
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 5 · 2023: 1 · 2022: 2 · 2021: 2 · 2020: 3 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 9 · 2015: 4
- FWCI
- 8.04
- Type
- book chapter
- Language
- en
- Open access
- closed
- Locations
- Progress in molecular biology and translational science (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › ATP Synthase and ATPases Research
- Keywords
- mitochondrial dynamics, mitochondrial fusion, mitochondrial fission, mitochondrial biogenesis, mitochondrial trafficking, motor proteins, mitochondrial DNA mutations, reactive oxygen species, neurodegeneration, aging, autophagy, calcium regulation, ATP production, electron transport chain
- MeSH terms
- Aging, Animals, Humans, Mitochondrial Proteins, Mitochondrial Diseases, Mitochondrial Membranes, Mitochondrial Size, Mitochondrial Dynamics
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