Decline in telomere length with increasing age across nonhuman vertebrates: A meta‐analysis

Author(s):  
Florentin Remot ◽  
Victor Ronget ◽  
Hannah Froy ◽  
Benjamin Rey ◽  
Jean‐Michel Gaillard ◽  
...  
2021 ◽  
Author(s):  
Li Lin ◽  
Kang Qin ◽  
Dezhong Chen ◽  
Ciyong Lu ◽  
Weiqing Chen ◽  
...  

2016 ◽  
Vol 54 ◽  
pp. 158-169 ◽  
Author(s):  
Maya B. Mathur ◽  
Elissa Epel ◽  
Shelley Kind ◽  
Manisha Desai ◽  
Christine G. Parks ◽  
...  

2018 ◽  
Vol 270 ◽  
pp. 41-49 ◽  
Author(s):  
Yu-Chi Huang ◽  
Liang-Jen Wang ◽  
Ping-Tao Tseng ◽  
Chi-Fa Hung ◽  
Pao-Yen Lin

2011 ◽  
Author(s):  
Ingrid M. Wentzensen ◽  
Lisa Mirabello ◽  
Ruth M. Pfeiffer ◽  
Sharon A. Savage

2020 ◽  
Vol 47 (9) ◽  
pp. 7181-7188 ◽  
Author(s):  
M. Lulkiewicz ◽  
J. Bajsert ◽  
P. Kopczynski ◽  
W. Barczak ◽  
B. Rubis

Abstract Telomerase is perceived as an immortality enzyme that might provide longevity to cells and whole organisms. Importantly, it is generally inactive in most somatic cells of healthy, adult men. Consequently, its substrates, i.e. telomeres, get shorter in most human cells with time. Noteworthy, cell life limitation due to telomere attrition during cell divisions, may not be as bad as it looks since longer cell life means longer exposition to harmful factors. Consequently, telomere length (attrition rate) becomes a factor that is responsible for inducing the signaling that leads to the elimination of cells that lived long enough to acquire severe damage. It seems that telomere length that depends on many different factors (including telomerase activity but also genetic factors, a hormonal profile that reflects sex, etc.) might become a useful marker of aging and exposition to stress. Thus in the current paper, we review the factors that affect telomere length in human cells focusing on sex that all together with different environmental and hormonal regulations as well as parental aspect affect telomere attrition rate. We also raise some limitations in the assessment of telomere length that hinders a trustworthy meta-analysis that might lead to acknowledgment of the real value of this parameter.


2019 ◽  
Vol 215 ◽  
pp. 64-74.e6 ◽  
Author(s):  
Zhongzheng Niu ◽  
Karen Li ◽  
Chuanbo Xie ◽  
Xiaozhong Wen

2019 ◽  
Vol 6 (10) ◽  
pp. 190937 ◽  
Author(s):  
Melissa Bateson ◽  
Dan T. A. Eisenberg ◽  
Daniel Nettle

Longitudinal studies have sought to establish whether environmental exposures such as smoking accelerate the attrition of individuals' telomeres over time. These studies typically control for baseline telomere length (TL) by including it as a covariate in statistical models. However, baseline TL also differs between smokers and non-smokers, and telomere attrition is spuriously linked to baseline TL via measurement error and regression to the mean. Using simulated datasets, we show that controlling for baseline TL overestimates the true effect of smoking on telomere attrition. This bias increases with increasing telomere measurement error and increasing difference in baseline TL between smokers and non-smokers. Using a meta-analysis of longitudinal datasets, we show that as predicted, the estimated difference in telomere attrition between smokers and non-smokers is greater when statistical models control for baseline TL than when they do not, and the size of the discrepancy is positively correlated with measurement error. The bias we describe is not specific to smoking and also applies to other exposures. We conclude that to avoid invalid inference, models of telomere attrition should not control for baseline TL by including it as a covariate. Many claims of accelerated telomere attrition in individuals exposed to adversity need to be re-assessed.


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