The role of mitochondria in ageing and carcinogenesis
Open accessAbstract
Mitochondria can perform multiple cellular functions including energy production, cell proliferation and apoptosis. These organelles contain their own genetic material, mitochondrial DNA (mtDNA), which is maternally inherited. Although much smaller than the nuclear genome, mtDNA is equally important, as it has been hypothesized to play a crucial role in ageing and carcinogenesis. This is partly due to the fact that mitochondria represent the major site for the generation of cellular oxidative stress and play a key role in mediating programmed cell death (apoptosis). Damage to mtDNA is therefore an important contributor to human ageing, cancer and neurodegenerative diseases. The most relevant footprints of mtDNA damage are point mutations of single bases, or deletions of the 16.5-kb mitochondrial genome. This review will focus on the key roles of mitochondrial function and mtDNA in oxidative stress production and as a mediator of apoptosis, and on the use of mtDNA as a biomarker of sun exposure. This will be related to the contribution of mitochondria and mtDNA in the ageing process and cancer, with a specific focus on human skin. In conclusion, it is likely that the interplay between nuclear and mitochondrial genes may hold the final understanding of the mitochondrial role in these disease processes.
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Mitochondria are dynamic organelles found within the cytoplasm of eukaryotic cells, and are responsible for the production of the majority (approximately 90%) of cellular energy via oxidative phosphorylation and the electron transport chain (ETC), in the form of adenosine triphosphate (ATP).
“There are a large number of studies into how and why we age that involve the mitochondria which are dynamic organelles found within the cytoplasm of eukaryotic cells, and are responsible for the production of the majority (approximately 90%) of cellular energy via oxidative phosphorylation and the electron transport chain (ETC), in the form of adenosine triphosphate (ATP) [Birch-Machin 2006].”
From Oxidative stress and ageing (2016) · cites this paper as Birch-Machin 2006
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“The mitochondrial membrane potential has also been shown to be decreased with age in specific tissues, as has the ATP-producing capability of mitochondria.”
BackgroundInfluentialBirket, M. J., Passos, J. F., von Zglinicki, T., & Birch-Machin, M. A. (2009) · Journal of Investigative Dermatology · doi:10.1038/jid.2008.373 · Cited by 24 · see citing works
Self-citation
- Authors
- Birch-Machin, M. A.
- Affiliations
- Newcastle University (GB)
- Corresponding author
- Birch-Machin, M. A.
- ORCID
- Birch-Machin, M. A.
- Venue
- Clinical and Experimental Dermatology
- Publisher
- Oxford University Press (OUP)
- Published
- 2006-06
- Volume
- 31
- Issue
- 4
- Pages
- 548-552
- ISSN
- 0307-6938 (ISSN-L)
- 1365-2230
- OpenAlex
- W2126963475
- Cited by
- 130
- References
- 34
- Citations by year
- 2025: 4 · 2024: 4 · 2023: 8 · 2022: 3 · 2021: 3 · 2020: 1 · 2019: 9 · 2018: 3 · 2017: 6 · 2016: 10 · 2015: 7 · 2014: 5 · 2013: 6 · 2012: 9
- FWCI
- 0.77
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Locations
- Clinical and Experimental Dermatology (publishedVersion)
- PubMed (publishedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Dermatology › Skin Protection and Aging
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- mitochondria, mitochondrial DNA, aging, carcinogenesis, oxidative stress, apoptosis, mitochondrial DNA damage, skin cancer, neurodegenerative diseases
- MeSH terms
- Aging, DNA Damage, DNA, Mitochondrial, Humans, Neoplasms, Ultraviolet Rays, Apoptosis, Reactive Oxygen Species, Oxidative Stress, Genes, Mitochondrial
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