Cellular Senescence in Ageing, Age-Related Disease and Longevity

ISSN: 1875-6212 (Online)
ISSN: 1570-1611 (Print)


Volume 12, 6 Issues, 2014


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Editor-in-Chief:
Dimitri P. Mikhailidis
Academic Head, Deptartment of Clinical Biochemistry
Royal Free Hospital Campus
University College London Medical School
University College London (UCL)
Pond Street
London, NW3 2QG
UK


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Cellular Senescence in Ageing, Age-Related Disease and Longevity

Author(s): Ewa Sikora, Anna Bielak-Zmijewska and Grazyna Mosieniak

Affiliation: Department of Biochemistry, Nencki Institute of Experimental Biology, Polish Academy of Sciences, 3 Pasteur St., 02-093 Warsaw, Poland.

Abstract

Cellular senescence is the state of permanent inhibition of cell proliferation. Senescent cells are characterized by several features including increased activity of senescence-associated β-galactosidase (SA-β-GAL) and senescenceassociated secretory phenotype (SASP). In vitro, 2 types of senescence have been described. One is telomere-dependent replicative senescence and the second is stress-induced premature senescence (SIPS). Despite some tissue-specific characteristics many kinds of cells, including stem/progenitor cells, can undergo senescence both in vitro and in vivo. Senescent cells were detected in murine, primate and human tissues using different markers. There is mounting evidence that senescent cells contribute to ageing and age-related disease by generating a low grade inflammation state (senescenceassociated secretory phenotype-SASP). Even though cellular senescence is a barrier for cancer it can, paradoxically, stimulate development of cancer via proinflammatory cytokines. There is evidence that senescent vascular cells, both endothelial and smooth muscle cells, participate in atherosclerosis and senescent preadipocytes and adipocytes have been shown to lead to insulin resistance. Thus, modulation of cellular senescence is considered as a potential pro-longevity strategy. This can be achieved by: elimination of selected senescent cells, epigenetic reprogramming of senescent cells, preventing cellular senescence or influencing the secretory phenotype. Some pharmacological interventions have already shown promising results.

Keywords: Age-related disease, biomarkers, DNA damage, low-grade inflammation, secretory phenotype, senescence, telomeres.

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Article Details

Volume: 12
Issue Number: 5
First Page: 698
Last Page: 706
Page Count: 9
DOI: 10.2174/1570161111666131219094045
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