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      Telomere Biology and Human Phenotype

      review-article
      Author(s): 1 , 1 , 2 , 1 , *
      Publication date (Electronic):
      Journal: Cells
      Publisher: MDPI
      Keywords: telomeres, telomere length, aging, senescence

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          Abstract

          Telomeres are nucleoprotein structures that cap the end of each chromosome arm and function to maintain genome stability. The length of telomeres is known to shorten with each cell division and it is well-established that telomere attrition is related to replicative capacity in vitro. Moreover, telomere loss is also correlated with the process of aging in vivo. In this review, we discuss the mechanisms that lead to telomere shortening and summarise telomere homeostasis in humans throughout a lifetime. In addition, we discuss the available evidence that shows that telomere shortening is related to human aging and the onset of age-related disease.

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          Cellular senescence in aging and age-related disease: from mechanisms to therapy.

          Bennett Childs, Matej Durik, Darren J. Baker … (2015)
          Cellular senescence, a process that imposes permanent proliferative arrest on cells in response to various stressors, has emerged as a potentially important contributor to aging and age-related disease, and it is an attractive target for therapeutic exploitation. A wealth of information about senescence in cultured cells has been acquired over the past half century; however, senescence in living organisms is poorly understood, largely because of technical limitations relating to the identification and characterization of senescent cells in tissues and organs. Furthermore, newly recognized beneficial signaling functions of senescence suggest that indiscriminately targeting senescent cells or modulating their secretome for anti-aging therapy may have negative consequences. Here we discuss current progress and challenges in understanding the stressors that induce senescence in vivo, the cell types that are prone to senesce, and the autocrine and paracrine properties of senescent cells in the contexts of aging and age-related diseases as well as disease therapy.
          Article 0 comments Cited 848 times – based on 0 reviews     Review now
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            Mitochondrial Dysfunction Induces Senescence with a Distinct Secretory Phenotype.

            Christopher D Wiley, Michael Velarde, Pacome Lecot … (2016)
            Cellular senescence permanently arrests cell proliferation, often accompanied by a multi-faceted senescence-associated secretory phenotype (SASP). Loss of mitochondrial function can drive age-related declines in the function of many post-mitotic tissues, but little is known about how mitochondrial dysfunction affects mitotic tissues. We show here that several manipulations that compromise mitochondrial function in proliferating human cells induce a senescence growth arrest with a modified SASP that lacks the IL-1-dependent inflammatory arm. Cells that underwent mitochondrial dysfunction-associated senescence (MiDAS) had lower NAD+/NADH ratios, which caused both the growth arrest and prevented the IL-1-associated SASP through AMPK-mediated p53 activation. Progeroid mice that rapidly accrue mtDNA mutations accumulated senescent cells with a MiDAS SASP in vivo, which suppressed adipogenesis and stimulated keratinocyte differentiation in cell culture. Our data identify a distinct senescence response and provide a mechanism by which mitochondrial dysfunction can drive aging phenotypes.
            Article 0 comments Cited 443 times – based on 0 reviews     Review now
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              Obesity, cigarette smoking, and telomere length in women.

              A Valdes, T. Andrew, J. P. Gardner … (2005)
              Obesity and smoking are important risk factors for many age-related diseases. Both are states of heightened oxidative stress, which increases the rate of telomere erosion per replication, and inflammation, which enhances white blood cell turnover. Together, these processes might accelerate telomere erosion with age. We therefore tested the hypothesis that increased body mass and smoking are associated with shortened telomere length in white blood cells. We investigated 1122 white women aged 18-76 years and found that telomere length decreased steadily with age at a mean rate of 27 bp per year. Telomeres of obese women were 240 bp shorter than those of lean women (p=0.026). A dose-dependent relation with smoking was recorded (p=0.017), and each pack-year smoked was equivalent to an additional 5 bp of telomere length lost (18%) compared with the rate in the overall cohort. Our results emphasise the pro-ageing effects of obesity and cigarette smoking.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cells
                Journal ID (iso-abbrev): Cells
                Journal ID (publisher-id): cells
                Title: Cells
                Publisher: MDPI
                ISSN (Electronic): 2073-4409
                Publication date (Electronic): 19 January 2019
                Publication date Collection: January 2019
                Volume: 8
                Issue: 1
                Electronic Location Identifier: 73
                Affiliations
                [1 ]University of Kent, School of Biosciences, Giles Lane, Canterbury, Kent, CT2-7NJ, UK; k.j.turner-24@ 123456kent.ac.uk (K.J.T.); vimal.vasu@ 123456nhs.net (V.V.)
                [2 ]Department of Child Health, East Kent Hospitals University Foundation NHS Trust, William Harvey Hospital, Ashford, Kent, TN24-0LZ, UK
                Author notes
                [* ]Correspondence: d.k.griffin@ 123456kent.ac.uk ; Tel.: +44-(0)1227-823-022
                Author information
                https://orcid.org/0000-0003-2606-9797
                https://orcid.org/0000-0001-7595-3226
                Article
                Publisher ID: cells-08-00073
                DOI: 10.3390/cells8010073
                PMC ID: 6356320
                PubMed ID: 30669451
                SO-VID: 35c36844-cea7-4984-8fc4-801f3fc96b22
                Copyright © © 2019 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 24 December 2018
                Date accepted : 16 January 2019
                Categories
                Subject: Review

                Keywords: telomeres,telomere length,aging,senescence
                Data availability:
                Keywords: telomeres, telomere length, aging, senescence

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