Author: Jacome-Burbano MS1, Gilson E2
Affiliation: <sup>1</sup>Université Côte d'Azur, Nice, France CNRS, Inserm, Institut for Research on Cancer and Aging, Nice (IRCAN), France.
<sup>2</sup>Université Côte d'Azur, Nice, France CNRS, Inserm, Institut for Research on Cancer and Aging, Nice (IRCAN), France; Department of Medical Genetics, Archet 2 Hospital, FHU Oncoage, CHU of Nice, Nice, France. Electronic address: Eric.GILSON@univ-cotedazur.fr.
Conference/Journal: Mech Ageing Dev.
Date published: 2020 May 4
Other:
Volume ID: 111256 , Special Notes: doi: 10.1016/j.mad.2020.111256. [Epub ahead of print] , Word Count: 183
Senescence is a cellular response to stress for both dividing and post-mitotic cells. Noteworthy, long-lived post-mitotic cells (collectively named LLPMCs), which can live for decades in the organism, can exhibit a distinct type of cellular aging characterized by a progressive functional decline not associated to an overt senescence phenotype. The age-related drivers of senescence and aging in LLPMCs remain largely unknown. There is evidence that an increased production of reactive oxygen species (ROS) due to dysfunctional mitochondria, coupled with an inherent inability of cellular-degradation mechanisms to remove damaged molecules, is responsible for senescence and aging in LLPMC. Although telomeric DNA shortening, by nature linked to cell division, is generally not considered as a driver of LLPMC aging and senescence, we discuss recent reports revealing the existence of age-related telomere changes in LLPMC. These findings reveal unexpected roles for telomeres in LLPMC function and invite us to consider the hypothesis of a complex telomere clock involved in both dividing and non-dividing cell aging.
Copyright © 2020. Published by Elsevier B.V.
KEYWORDS: DNA damage; Long-lived post-mitotic cell (LLPMC); Mitochondrial dysfunction; Senescence; Telomeres
PMID: 32380018 DOI: 10.1016/j.mad.2020.111256