The DOI matches its Crossref record; 82 of the 83 references it cites were found in a registry or an index.
Mitochondrial quality control: an integrated network of pathways
Abstract
Mitochondria are organelles of eukaryotic cells with various functions. Best known is their role in energy transduction leading to the formation of ATP. As byproducts of this process, reactive oxygen species (ROS) are formed that can damage different types of molecules leading to mitochondrial dysfunction. Different quality control (QC) mechanisms keep mitochondria functional. Although several components involved in mitochondrial QC have been characterized in some detail, others remain to be integrated into what is currently emerging as a hierarchical network of interacting pathways. The elucidation of this network holds the key to the understanding of complex biological processes such as aging and the development of age-related diseases.
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In the citing paper
“However, with increasing mitochondria, the level of ROS is also increased as mitochondrial byproducts, which can result in oxidative damage of mitochondria [176].”
From AMPK, Mitochondrial Function, and Cardiovascular Disease (2020) · cites this paper as [176]
In the citing paper
“Since ROS are important signalling molecules [Desler et al., 2011; Fischer et al., 2012], the dose and target of the administered antioxidant would have to be considered to prevent the alteration of cellular homeostasis.”
From Oxidative stress and ageing (2016) · cites this paper as Fischer et al., 2012
Citations
Cites
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
ROS as signalling molecules: Mechanisms that generate specificity in ROS homeostasis
D'Autréaux, B., & Toledano, M. B. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2256 · Cited by 3,642
Youle, R. J., & Narendra, D. P. (2011) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3028 · Cited by 3,273
Fission and selective fusion govern mitochondrial segregation and elimination by autophagy
Twig, G., Elorza, A., Molina, A. J. A., Mohamed, H., Wikstrom, J. D., Walzer, G., Stiles, L., Haigh, S. E., Katz, S., Las, G., et al. (2008) · The EMBO Journal · doi:10.1038/sj.emboj.7601963 · Cited by 3,082
PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin
Narendra, D. P., Jin, S. M., Tanaka, A., Suen, D.-F., Gautier, C. A., Shen, J., Cookson, M. R., & Youle, R. J. (2010) · PLoS Biology · doi:10.1371/journal.pbio.1000298 · Cited by 2,944
PINK1/Parkin-mediated mitophagy is dependent on VDAC1 and p62/SQSTM1
Geisler, S., Holmström, K. M., Skujat, D., Fiesel, F. C., Rothfuss, O. C., Kahle, P. J., & Springer, W. (2010) · Nature Cell Biology · doi:10.1038/ncb2012 · Cited by 2,835
The Biologic Clock: The Mitochondria?
Harman, D. (1972) · Journal of the American Geriatrics Society · doi:10.1111/j.1532-5415.1972.tb00787.x · Cited by 2,026
Mitochondrial fusion and fission in cell life and death
Westermann, B. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm3013 · Cited by 2,002
Matsuda, N., Sato, S., Shiba, K., Okatsu, K., Saisho, K., Gautier, C. A., Sou, Y.-S., Saiki, S., Kawajiri, S., Sato, F., et al. (2010) · Journal of Cell Biology · doi:10.1083/jcb.200910140 · Cited by 1,969
PINK1-dependent recruitment of Parkin to mitochondria in mitophagy
Vives-Bauza, C., Zhou, C., Huang, Y., Cui, M., de Vries, R. L. A., Kim, J., May, J., Tocilescu, M. A., Liu, W., Ko, H. S., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0911187107 · Cited by 1,616
Cited by
Sorted by citations
Mitochondria dysfunction in the pathogenesis of Alzheimer’s disease: Recent advances.
Wang, W., Zhao, F., Ma, X., Perry, G., & Zhu, X. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00376-6 · Cited by 1,274
Mitochondrial dynamics, mitophagy and cardiovascular disease
Vásquez-Trincado, C., García‐Carvajal, I., Pennanen, C., Parra, V., Hill, J. A., Rothermel, B. A., & Lavandero, S. (2015) · The Journal of Physiology · doi:10.1113/jp271301 · Cited by 637
Mitochondria as a Target of Environmental Toxicants
Meyer, J. N., Leung, M. C. K., Rooney, J. P., Sendoel, A., Hengartner, M. O., Kisby, G. E., & Bess, A. S. (2013) · Toxicological Sciences · doi:10.1093/toxsci/kft102 · Cited by 587
Mitochondrial Dysfunction and Biogenesis in Neurodegenerative diseases: Pathogenesis and Treatment
Golpich, M., Amini, E., Mohamed, Z., Raymond, A. A., Ibrahim, N. M., & Ahmadiani, A. (2016) · CNS Neuroscience & Therapeutics · doi:10.1111/cns.12655 · Cited by 555
Drug-induced mitochondrial dysfunction and cardiotoxicity
Varga, Z. V., Ferdinandy, P., Liaudet, L., & Pacher, P. (2015) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00554.2015 · Cited by 547
Metadata
- Authors
- Fischer, F., Hamann, A., & Osiewacz, H. D.
- Affiliations
- Goethe University Frankfurt (DE)
- Corresponding author
- Osiewacz, Heinz D.
- Venue
- Trends in Biochemical Sciences
- Publisher
- Elsevier BV
- Published
- 2012-07
- Volume
- 37
- Issue
- 7
- Pages
- 284-292
- ISSN
- 0968-0004 (ISSN-L)
- OpenAlex
- W2043062268
- Cited by
- 248
- References
- 83
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 17 · 2023: 14 · 2022: 21 · 2021: 20 · 2020: 26 · 2019: 15 · 2018: 19 · 2017: 14 · 2016: 10 · 2015: 22 · 2014: 19 · 2013: 19 · 2012: 8
- FWCI
- 1.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Trends in Biochemical Sciences (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- 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 › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondrial quality control, mitochondrial dysfunction, reactive oxygen species, oxidative damage, energy transduction, ATP production, aging, age-related diseases, mitochondrial biogenesis, organelle homeostasis
- MeSH terms
- Aging, Animals, Humans, Mitochondria, Signal Transduction, Reactive Oxygen Species
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