Telomere length: how the length makes a difference
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REVIEW
Telomere length: how the length makes a difference M. Lulkiewicz1 · J. Bajsert1 · P. Kopczynski2 · W. Barczak3,4 · B. Rubis1 Received: 19 December 2019 / Accepted: 23 May 2020 © The Author(s) 2020
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. Keywords Telomeres · Telomerase · Immortality · Aging · Sex · Hormones
Introduction Telomere dynamics is associated with aging and senescence. Both terms often appear together, but they describe a bit different set of metabolic changes. Aging is the attenuation of physiological functions that comes with time and, eventually, leads to cell death. Primary drivers of aging are telomere damage, epigenetic dysregulation, DNA damage, and mitochondrial dysfunction. Noteworthy, aging is the major risk factor for cancer, cardiovascular disease, diabetes, and * B. Rubis [email protected] 1
Department of Clinical Chemistry and Molecular Diagnostics, Poznan University of Medical Sciences, 49 Przybyszewskiego St., 60‑355 Poznan, Poland
2
Centre for Orthodontic Mini‑Implants at the Department and Clinic of Maxillofacial Orthopedics and Orthodontics, Poznan University of Medical Sciences, 60‑812 Poznan, Poland
3
Department of Head and Neck Surgery, Poznan University of Medical Sciences, The Greater Poland Cancer Centre, 61‑866 Poznan, Poland
4
Radiobiology Laboratory, Department of Medical Physics, The Greater Poland Cancer Centre, 61‑866 Poznan, Poland
neurodegenerative disorders as well as chronic obstructive pulmonary disease, chronic kidney disease, osteoporosis, sarcopenia, stroke and many others [1]. Consequently, some of these drivers can induce senescence that is the process of stable, irreversible growth arrest of cells. Apart from evident changes in the phenotype of an organism, senescence also causes
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