Lifestyle impacts on the aging-associated expression of biomarkers of DNA damage and telomere dysfunction in human blood
Open accessAbstract
Cellular aging is characterized by telomere shortening, which can lead to uncapping of chromosome ends (telomere dysfunction) and activation of DNA damage responses. There is some evidence that DNA damage accumulates during human aging and that lifestyle factors contribute to the accumulation of DNA damage. Recent studies have identified a set of serum markers that are induced by telomere dysfunction and DNA damage, and these markers showed an increased expression in blood during human aging. Here, we investigated the influence of lifestyle factors (such as exercise, smoking, body mass) on the aging-associated expression of serum markers of DNA damage (CRAMP, EF-1alpha, stathmin, n-acetyl-glucosaminidase and chitinase) in comparison with other described markers of cellular aging (p16(INK4a) upregulation and telomere shortening) in human peripheral blood. The study shows that lifestyle factors have an age-independent impact on the expression level of biomarkers of DNA damage. Smoking and increased body mass indices were associated with elevated levels of biomarkers of DNA damage independent of the age of the individuals. In contrast, exercise was associated with an age-independent reduction in the expression of biomarkers of DNA damage in human blood. The expression of biomarkers of DNA damage correlated positively with p16(INK4a) expression and negatively with telomere length in peripheral blood T-lymphocytes. Together, these data provide experimental evidence that both aging and lifestyle impact on the accumulation of DNA damage during human aging.
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In a subset (n = 136) of human samples from the same cohort, relatively higher levels of habitual activity were associated with lower levels of P16 in circulating T cells.
“A similar study in a subset (n = 136) of human samples from the same cohort corroborated these findings, showing relatively higher levels of habitual activity were associated with lower levels of P16 in circulating T cells (61).”
From Exercise Counters the Age-Related Accumulation of Senescent Cells (2022) · cites this paper as [61]
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- Authors
- Song, Z., Von Figura, G., Liu, Y., Kraus, J. M., Torrice, C., Dillon, P., Rudolph‐Watabe, M., Ju, Z., Kestler, H. A., Sanoff, H., & Lenhard Rudolph, K.
- Affiliations
- Universität Ulm (DE)
- University of North Carolina at Chapel Hill (US)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- University of Virginia (US)
- Corresponding author
- Kestler, Hans A.
- Venue
- Aging Cell
- Publisher
- Wiley
- Published
- 2010-07-21
- Volume
- 9
- Issue
- 4
- Pages
- 607-615
- ISSN
- 1474-9718 (ISSN-L)
- 1474-9726
- PMC
- PMC2910221
- OpenAlex
- W1600919571
- Cited by
- 163
- References
- 45
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 7 · 2023: 8 · 2022: 11 · 2021: 8 · 2020: 17 · 2019: 14 · 2018: 14 · 2017: 13 · 2016: 12 · 2015: 9 · 2014: 17 · 2013: 6 · 2012: 9
- FWCI
- 4.98
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Aging Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- National Institutes of Health (5r01ag024379-15)
- National Institute on Aging (AG024379, R01-AG024379)
- 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 › Epigenetics and DNA Methylation
- Keywords
- cellular aging, DNA damage, telomere dysfunction, telomere shortening, lifestyle factors, physical activity, smoking, body mass index, serum biomarkers, cramps, EF-1α, stathmin, N-acetyl-beta-D-glucosaminidase, chitinase, p16INK4a, telomere length, T cells, DNA damage response
- MeSH terms
- Aging, DNA Damage, Humans, Life Style, Regression Analysis, Smoking, T-Lymphocytes, Biomarkers, Exercise, Body Mass Index, Telomere, Cellular Senescence
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