Demystifying the role of mitochondria in senescence
Open accessAbstract
In a study published in The EMBO Journal, we demonstrated that mitochondria are necessary for the proinflammatory phenotype of senescence. Furthermore, we identified a new senescence-regulatory pathway involving mTOR-dependent mitochondrial biogenesis. These data highlight mitochondria as targets for interventions that counteract the pro-aging effects of senescence while preserving tumor suppression.
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Damaged mitochondrial DNA alters oxidative phosphorylation reactions and can further enhance ROS production.
“In turn, damaged mitochondrial DNA alters oxidative phosphorylation reactions and can further enhance ROS production [269].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [269]
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Cites
Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype
Wiley, C. D., Velarde, M. C., Lecot, P., Liu, S., Sarnoski, E. A., Freund, A., Shirakawa, K., Lim, H. W., Davis, S. S., Ramanathan, A., et al. (2016) · Cell Metabolism · doi:10.1016/j.cmet.2015.11.011 · Cited by 1,275 · cited 1× · see citing works
“Recently, it was shown that mitochondrial dysfunction resulted in senescence with a distinct type of SASP, which lacks the IL-1/NF-kB activation characteristic of other senescent types.(10) Further work will be needed to integrate these new findings and identify which mitochondrial signals trigger the senescence progr…”
BackgroundLaberge, R.-M., Sun, Y., Orjalo, A. V., Patil, C. K., Freund, A., Zhou, L., Curran, S. C., Davalos, A. R., Wilson-Edell, K. A., Liu, S., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3195 · Cited by 1,160 · see citing works
Feedback between p21 and reactive oxygen production is necessary for cell senescence
Passos, J. F., Nelson, G., Wang, C., Richter, T., Simillion, C., Proctor, C. J., Miwa, S., Olijslagers, S., Hallinan, J., Wipat, A., et al. (2010) · Molecular Systems Biology · doi:10.1038/msb.2010.5 · Cited by 1,019 · cited 1× · see citing works
“metabolism occurred in parallel with an increased mitochondrial mass driven by mitochondrial biogenesis.(3) This led us to hypothesize that increased mitochondrial content might be an inducer of senescence.”
BackgroundSelf-citationMitochondria are required for pro-ageing features of the senescent phenotype
Correia‐Melo, C., Marques, F. D., Anderson, R., Hewitt, G., Hewitt, R., Cole, J., Carroll, B. M., Miwa, S., Birch, J., Merz, A., et al. (2016) · The EMBO Journal · doi:10.15252/embj.201592862 · Cited by 796 · see citing works
Self-citationmTOR regulates MAPKAPK2 translation to control the senescence-associated secretory phenotype
Herranz, N., Gallage, S., Mellone, M., Wuestefeld, T., Klotz, S., Hanley, C. J., Raguz, S., Acosta, J. C., Innes, A. J., Banito, A., et al. (2015) · Nature Cell Biology · doi:10.1038/ncb3225 · Cited by 788 · see citing works
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Research works printed but not linked: 5
- van Deursen JM. The role of senescent cells in ageing. Nature 2014; 509:439-46; PMID:24848057; http://dx.doi.org/10.1038/nature13193 · DOI · Paper page
- Hewitt G, Jurk D, Marques FDM, Correia-Melo C, Hardy T, Gackowska A, et al. Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence. Nat Commun 2012; 3:708; PMID:22426229; http://dx.doi.org/10.1038/ncomms1708 · DOI · Paper page
- Correia-Melo C, Passos JF. Mitochondria: Are they causal players in cellu- lar senescence? Biochimica et Biophysica Acta (BBA) -Bioenergetics 2015; 1847:1373-9; PMID:26028303; http://dx.doi.org/10.1016/j. bbabio.2015.05.017 · DOI · Paper page
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Mechanisms and Regulation of Cellular Senescence
Roger, L., Tomas, F., & Gire, V. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms222313173 · Cited by 395 · see citing works
- Authors
- Correia-Melo, C., & Passos, J. F.
- Affiliations
- Institute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University, Newcastle upon Tyne, United Kingdom
- Newcastle University (GB)
- Corresponding author
- Passos, João F.
- ORCID
- Passos, João F.
- Venue
- Molecular & Cellular Oncology
- Publisher
- Informa UK Limited
- Published
- 2016-06-09
- Volume
- 3
- Issue
- 4
- Pages
- e1162896
- ISSN
- 2372-3548 (ISSN-L)
- 2372-3556
- PMC
- PMC4972119
- OpenAlex
- W2334281150
- Cited by
- 5
- References
- 5
- Citations by year
- 2024: 1 · 2021: 1 · 2019: 2 · 2017: 1
- FWCI
- 0.80
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular & Cellular Oncology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council (MR/K006312/1)
- Biotechnology and Biological Sciences Research Council (BB/K017314/1, BB/H022384/1)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- cellular senescence, mitochondria, pro-inflammatory phenotype, mTOR, mitochondrial biogenesis, aging, tumor suppression, senescence-associated inflammation
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