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Irreparable telomeric DNA damage and persistent DDR signalling as a shared causative mechanism of cellular senescence and ageing.

作者信息

Rossiello Francesca, Herbig Utz, Longhese Maria Pia, Fumagalli Marzia, d'Adda di Fagagna Fabrizio

机构信息

IFOM Foundation - FIRC Institute of Molecular Oncology Foundation, Milan 20139, Italy.

Department of Microbiology and Molecular Genetics, New Jersey Medical School - Cancer Center, Rutgers Biomedical and Health Sciences, Rutgers University, Newark, NJ 07103, USA.

出版信息

Curr Opin Genet Dev. 2014 Jun;26:89-95. doi: 10.1016/j.gde.2014.06.009. Epub 2014 Aug 11.

DOI:10.1016/j.gde.2014.06.009
PMID:25104620
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4217147/
Abstract

The DNA damage response (DDR) orchestrates DNA repair and halts cell cycle. If damage is not resolved, cells can enter into an irreversible state of proliferative arrest called cellular senescence. Organismal ageing in mammals is associated with accumulation of markers of cellular senescence and DDR persistence at telomeres. Since the vast majority of the cells in mammals are non-proliferating, how do they age? Are telomeres involved? Also oncogene activation causes cellular senescence due to altered DNA replication and DDR activation in particular at the telomeres. Is there a common mechanism shared among apparently distinct types of cellular senescence? And what is the role of telomeric DNA damage?

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b504/4217147/1a57cc4ad9dc/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b504/4217147/f072b6763bdf/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b504/4217147/1a57cc4ad9dc/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b504/4217147/f072b6763bdf/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b504/4217147/1a57cc4ad9dc/gr2.jpg

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本文引用的文献

[1]
A complex secretory program orchestrated by the inflammasome controls paracrine senescence.

Nat Cell Biol. 2013-6-16

[2]
End-joining inhibition at telomeres requires the translocase and polySUMO-dependent ubiquitin ligase Uls1.

EMBO J. 2013-2-15

[3]
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Mol Cell. 2012-8-24

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Ann N Y Acad Sci. 2012-8

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DNA Repair (Amst). 2012-8-11

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Nature. 2012-8-9

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Oncogene-induced telomere dysfunction enforces cellular senescence in human cancer precursor lesions.

EMBO J. 2012-5-8

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Science. 2012-5-4

[9]
A role for small RNAs in DNA double-strand break repair.

Cell. 2012-3-22

[10]
Telomeres are favoured targets of a persistent DNA damage response in ageing and stress-induced senescence.

Nat Commun. 2012-2-28

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