Lifestyle impacts on the aging‐associated expression of biomarkers of DNA damage and telomere dysfunction in human blood |
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| Authors: | Zhangfa Song Guido Von Figura Yan Liu Johann M. Kraus Chad Torrice Patric Dillon Masami Rudolph‐Watabe Zhenyu Ju Hans A. Kestler Hanna Sanoff Karl Lenhard Rudolph |
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| Affiliation: | 1. Institute of Molecular Medicine and Max‐Planck Research Group on Stem Cell Aging, University of Ulm, Ulm, Germany;2. Department of Colorectal Surgery, Sir Run Run Shaw Hospital, Zhejiang University, Hangzhou, China;3. These authors contributed equally.;4. Department of Genetics, University of North Carolina School of Medicine, Chapel Hill, NC, USA;5. Department of Internal Medicine I, University of Ulm, Ulm, Germany;6. Research group of Bioinformatics and Systems Biology, Institute of Neural Information Processing University of Ulm, Ulm, Germany;7. Department of Otorhinolaryngology, University of Ulm, Ulm, Germany;8. Max‐Planck‐Partner Group on Stem Cell aging, Key laboratory of Human Diseases Comparative Medicine Ministry of Health Institute of Laboratory Animal Sciences, Chinese Academy of Medical Sciences, Beijing, China;9. Department of Medicine, University of Virginia Charlottesville, VA, USA |
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| Abstract: | 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‐1α, stathmin, n‐acetyl‐glucosaminidase and chitinase) in comparison with other described markers of cellular aging (p16INK4a 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 p16INK4a 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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| Keywords: | Aging marker DNA damage telomere dysfunction senescence serum markers lifestyle |
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