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      Telomeres: beacons of autocrine and paracrine DNA damage during skin aging

      review-article
      a , a , b
      Cell Cycle
      Taylor & Francis
      Senescence, telomeres, aging, mitochondria

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          ABSTRACT

          Cellular senescence is an irreversible cell cycle arrest, which can be triggered by a number of stressors, including telomere damage. Among many other phenotypic changes, senescence is accompanied by increased secretion of pro-inflammatory molecules, also known as the senescence-associated secretory phenotype (SASP). It is thought that accumulation of senescent cells contributes to age-associated tissue dysfunction partly by inducing senescence in neighboring cells through mechanisms involving SASP factors. Here, we will review evidence suggesting that telomeres can become dysfunctional irrespectively of shortening, and that this may be a mechanism-driving senescence in post-mitotic or slow dividing cells. Furthermore, we review recent evidence that supports that senescent melanocytes induce paracrine telomere damage during skin aging, which may be the mechanism responsible for propagation of senescent cells. We propose that telomeres are sensors of imbalances in the cellular milieu and act as beacons of stress, contributing to autocrine and paracrine senescence.

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          Author and article information

          Journal
          Cell Cycle
          Cell Cycle
          KCCY
          kccy20
          Cell Cycle
          Taylor & Francis
          1538-4101
          1551-4005
          2020
          16 February 2020
          : 19
          : 5
          : 532-540
          Affiliations
          [a ] Department of Physiology and Biomedical Engineering, Mayo Clinic , Rochester, USA
          [b ] Institute for Cell and Molecular Biosciences, Newcastle University Institute for Ageing, Newcastle University , Newcastle upon Tyne, UK
          Author notes
          CONTACT João F. Passos Passos.Joao@ 123456mayo.edu
          Article
          PMC7100988 PMC7100988 7100988 1728016
          10.1080/15384101.2020.1728016
          7100988
          32065062
          8f23393a-f6ac-4039-a76e-7b4ecf5f72ef
          © 2020 Informa UK Limited, trading as Taylor & Francis Group
          History
          : 4 December 2019
          : 14 January 2020
          : 6 February 2020
          Page count
          Figures: 2, References: 66, Pages: 9
          Funding
          Funded by: Biotechnology and Biological Sciences Research Council 10.13039/501100000268
          Award ID: BB/L502066/1
          Funded by: Biotechnology and Biological Sciences Research Council 10.13039/501100000268
          Award ID: BB/K017314/1
          Funded by: Ted Nash Foundation
          Award ID: N/A
          This work was supported by the Biotechnology and Biological Sciences Research Council [BB/L502066/1]; Biotechnology and Biological Sciences Research Council [BB/K017314/1]; Ted Nash Foundation [N/A].
          Categories
          Review

          mitochondria,telomeres,aging,Senescence
          mitochondria, telomeres, aging, Senescence

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