DNA damage and ageing: New-age ideas for an age-old problem

George A. Garinis; Gijsbertus T.J. van der Horst; Jan Vijg; Jan H.J. Hoeijmakers

doi:10.1038/ncb1108-1241

DNA damage and ageing: New-age ideas for an age-old problem

George A. Garinis, Gijsbertus T.J. van der Horst, Jan Vijg, Jan H.J. Hoeijmakers

Genetics

Research output: Contribution to journal › Review article › peer-review

297 Scopus citations

Abstract

Loss of genome maintenance may causally contribute to ageing, as exemplified by the premature appearance of multiple symptoms of ageing in a growing family of human syndromes and in mice with genetic defects in genome maintenance pathways. Recent evidence revealed a similarity between such prematurely ageing mutants and long-lived mice harbouring mutations in growth signalling pathways. At first sight this seems paradoxical as they represent both extremes of ageing yet show a similar 'survival' response that is capable of delaying age-related pathology and extending lifespan. Understanding the mechanistic basis of this response and its connection with genome maintenance would open exciting possibilities for counteracting cancer or age-related diseases, and for promoting longevity.

Original language	English (US)
Pages (from-to)	1241-1247
Number of pages	7
Journal	Nature Cell Biology
Volume	10
Issue number	11
DOIs	https://doi.org/10.1038/ncb1108-1241
State	Published - 2008

ASJC Scopus subject areas

Cell Biology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1038/ncb1108-1241

Cite this

@article{ab296db6aa3f4f2694f7427437af9b9c,

title = "DNA damage and ageing: New-age ideas for an age-old problem",

abstract = "Loss of genome maintenance may causally contribute to ageing, as exemplified by the premature appearance of multiple symptoms of ageing in a growing family of human syndromes and in mice with genetic defects in genome maintenance pathways. Recent evidence revealed a similarity between such prematurely ageing mutants and long-lived mice harbouring mutations in growth signalling pathways. At first sight this seems paradoxical as they represent both extremes of ageing yet show a similar 'survival' response that is capable of delaying age-related pathology and extending lifespan. Understanding the mechanistic basis of this response and its connection with genome maintenance would open exciting possibilities for counteracting cancer or age-related diseases, and for promoting longevity.",

author = "Garinis, {George A.} and {van der Horst}, {Gijsbertus T.J.} and Jan Vijg and Hoeijmakers, {Jan H.J.}",

note = "Funding Information: This work was supported by the Netherlands Organization for Scientific Research (NWO) through the foundation of the Research Institute Diseases of the Elderly, as well as grants from SenterNovem IOP-Genomics (IGE03009), NIH (1PO1 AG17242-02), NIEHS (1UO1 ES011044), EC (QRTL-1999-02002), and the Dutch Cancer Society (EUR 99-2004).",

year = "2008",

doi = "10.1038/ncb1108-1241",

language = "English (US)",

volume = "10",

pages = "1241--1247",

journal = "Nature Cell Biology",

issn = "1465-7392",

publisher = "Nature Publishing Group",

number = "11",

}

TY - JOUR

T1 - DNA damage and ageing

T2 - New-age ideas for an age-old problem

AU - Garinis, George A.

AU - van der Horst, Gijsbertus T.J.

AU - Vijg, Jan

AU - Hoeijmakers, Jan H.J.

N1 - Funding Information: This work was supported by the Netherlands Organization for Scientific Research (NWO) through the foundation of the Research Institute Diseases of the Elderly, as well as grants from SenterNovem IOP-Genomics (IGE03009), NIH (1PO1 AG17242-02), NIEHS (1UO1 ES011044), EC (QRTL-1999-02002), and the Dutch Cancer Society (EUR 99-2004).

PY - 2008

Y1 - 2008

N2 - Loss of genome maintenance may causally contribute to ageing, as exemplified by the premature appearance of multiple symptoms of ageing in a growing family of human syndromes and in mice with genetic defects in genome maintenance pathways. Recent evidence revealed a similarity between such prematurely ageing mutants and long-lived mice harbouring mutations in growth signalling pathways. At first sight this seems paradoxical as they represent both extremes of ageing yet show a similar 'survival' response that is capable of delaying age-related pathology and extending lifespan. Understanding the mechanistic basis of this response and its connection with genome maintenance would open exciting possibilities for counteracting cancer or age-related diseases, and for promoting longevity.

AB - Loss of genome maintenance may causally contribute to ageing, as exemplified by the premature appearance of multiple symptoms of ageing in a growing family of human syndromes and in mice with genetic defects in genome maintenance pathways. Recent evidence revealed a similarity between such prematurely ageing mutants and long-lived mice harbouring mutations in growth signalling pathways. At first sight this seems paradoxical as they represent both extremes of ageing yet show a similar 'survival' response that is capable of delaying age-related pathology and extending lifespan. Understanding the mechanistic basis of this response and its connection with genome maintenance would open exciting possibilities for counteracting cancer or age-related diseases, and for promoting longevity.

UR - http://www.scopus.com/inward/record.url?scp=55549116359&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=55549116359&partnerID=8YFLogxK

U2 - 10.1038/ncb1108-1241

DO - 10.1038/ncb1108-1241

M3 - Review article

C2 - 18978832

AN - SCOPUS:55549116359

SN - 1465-7392

VL - 10

SP - 1241

EP - 1247

JO - Nature Cell Biology

JF - Nature Cell Biology

IS - 11

ER -

DNA damage and ageing: New-age ideas for an age-old problem

Abstract

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this