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Lifestyle impacts on the aging-associated expression of biomarkers of DNA damage and telomere dysfunction in human blood

机译:生活方式对人类血液中DNA损伤和端粒功能障碍生物标志物的衰老相关表达的影响

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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-1, stathmin, n-acetyl-glucosaminidase and chitinase) in comparison with other described markers of cellular aging (p16
机译:细胞衰老的特征是端粒缩短,这可能导致染色体末端解键(端粒功能障碍)和DNA损伤反应的激活。有证据表明,DNA损伤会在人类衰老过程中累积,生活方式因素会导致DNA损伤的积累。最近的研究已经鉴定出一组由端粒功能障碍和DNA损伤诱导的血清标志物,这些标志物显示了人类衰老过程中血液中表达的增加。在这里,我们比较了生活方式因素(例如运动,吸烟,体重)对DNA损伤血清标记物(CRAMP,EF-1,stathmin,n-乙酰氨基葡糖苷酶和几丁质酶)与衰老相关的表达的影响。以及其他描述的人类外周血细胞衰老标记(p16

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