Mitochondrial dysfunction and cell senescence — skin deep into mammalian aging
Open accessAbstract
Thus, we are again left with a chicken-and egg situation: Is disrupted Ca2+ signalling, reduced mTOR activity and increased autophagy found in SOD2-/- cells because there are more senescent cells in the examined population? Or is any of these factors the culprit that triggers senescence in the first place? While the answer to these questions still eludes us, the study from Campisi and colleagues highlights the importance of mitochondrial dysfunction and cellular senescence in vivo and its impact on the aging process.
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Increased aerobic glycolysis compensates for reduced ATP production caused by mitochondrial respiration decline during senescence.
“Increased aerobic glycolysis compensates for the reduced adenosine triphosphate (ATP) production caused by mitochondrial respiration decline during senescence [1,208,209,210].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [208]
In the early stage of senescence, mitochondria display impaired oxidative phosphorylation capacity and reduced inner membrane potential, resulting in ROS overproduction.
“In the early stage of senescence, mitochondria do not function properly and display impaired oxidative phosphorylation capacity and reduced inner membrane potential, resulting in ROS overproduction [120,121,208,211].”
From Mechanisms and Regulation of Cellular Senescence (2021) · cites this paper as [208]
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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 · see citing works
Self-citationMitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence
Passos, J. F., Saretzki, G., Ahmed, S., Nelson, G., Richter, T., Peters, H., Wappler, I., Birket, M. J., Harold, G., Schaeuble, K., et al. (2007) · PLoS Biology · doi:10.1371/journal.pbio.0050110 · Cited by 796 · see citing works
Self-citationVan Remmen, H., Ikeno, Y., Hamilton, M., Pahlavani, M., Wolf, N., Thorpe, S. R., Alderson, N. L., Baynes, J. W., Epstein, C. J., Huang, T.-T., et al. (2003) · Physiological Genomics · doi:10.1152/physiolgenomics.00122.2003 · Cited by 734 · see citing works
DNA damage response and cellular senescence in tissues of aging mice
Wang, C., Jurk, D., Maddick, M., Nelson, G., Martin‐Ruiz, C., & Von Zglinicki, T. (2009) · Aging Cell · doi:10.1111/j.1474-9726.2009.00481.x · Cited by 696 · see citing works
Self-citationVelarde, M. C., Flynn, J. M., Day, N. U., Melov, S., & Campisi, J. (2012) · Aging · doi:10.18632/aging.100423 · Cited by 299 · see citing works
The choice between p53-induced senescence and quiescence is determined in part by the mTOR pathway.
Korotchkina, L. G., Leontieva, O. V., Bukreeva, E. I., Demidenko, Z. N., Gudkov, A. V., & Blagosklonny, M. V. (2010) · Aging · doi:10.18632/aging.100160 · Cited by 278 · see citing works
Lipofuscin accumulation in proliferating fibroblasts in vitro: an indicator of oxidative stress
Sitte, N., Merker, K., Grune, T., & von Zglinicki, T. (2001) · Experimental Gerontology · doi:10.1016/s0531-5565(00)00253-9 · Cited by 127 · see citing works
Treiber, N., Maity, P., Singh, K., Kohn, M., Keist, A. F., Ferchiu, F., Sante, L., Frese, S., Bloch, W., Kreppel, F., et al. (2011) · Aging Cell · doi:10.1111/j.1474-9726.2010.00658.x · Cited by 109 · see citing works
Mitochondrial Reactive Oxygen Species in Mice Lacking Superoxide Dismutase 2
Morten, K., Ackrell, B. A. C., & Melov, S. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m509261200 · Cited by 61 · see citing works
Zhang, Y., Zhang, H., Shi, Y., Lustgarten, M. S., Li, Y., Qi, W., Zhang, B.-X., & Remmen, H. V. (2010) · Free Radical Biology and Medicine · doi:10.1016/j.freeradbiomed.2010.07.006 · Cited by 48 · see citing works
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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
Mitochondrial fragmentation in cigarette smoke-induced bronchial epithelial cell senescence
Hara, H., Araya, J., Ito, S., Kobayashi, K., Takasaka, N., Yoshii, Y., Wakui, H., Kojima, J., Shimizu, K., Numata, T., et al. (2013) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00146.2013 · Cited by 219 · see citing works
Involvement of PARK2-Mediated Mitophagy in Idiopathic Pulmonary Fibrosis Pathogenesis
Kobayashi, K., Araya, J., Minagawa, S., Hara, H., Saito, N., Kadota, T., Sato, N., Yoshida, M., Tsubouchi, K., Kurita, Y., et al. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1600265 · Cited by 145 · see citing works
- Authors
- Passos, J. F., & von Zglinicki, T.
- Affiliations
- Institute for Ageing and Health, Newcastle University, Newcastle upon Tyne, NE4 5PL, UK
- Venue
- Aging
- Publisher
- Impact Journals, LLC
- Published
- 2012-02-12
- Volume
- 4
- Issue
- 2
- Pages
- 74-75
- ISSN
- 1945-4589 (ISSN-L)
- PMC
- PMC3314168
- OpenAlex
- W1576167641
- Cited by
- 28
- References
- 10
- Citations by year
- 2026: 2 · 2024: 3 · 2023: 1 · 2022: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 2 · 2017: 1 · 2016: 4 · 2015: 4 · 2014: 2 · 2013: 1 · 2012: 3
- FWCI
- 2.13
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Aging (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Funders
- Biotechnology and Biological Sciences Research Council (BB/H022384/1, BB/I020748/1)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondrial dysfunction, cellular senescence, calcium signaling, mTOR, autophagy, skin aging, senolytic therapy
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