Age to survive: DNA damage and aging

Björn Schumacher; George A. Garinis; Jan H.J. Hoeijmakers

doi:10.1016/j.tig.2007.11.004

Age to survive: DNA damage and aging

Björn Schumacher, George A. Garinis, Jan H.J. Hoeijmakers

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

210 Citations (Scopus)

Abstract

Aging represents the progressive functional decline and increased mortality risk common to nearly all metazoans. Recent findings experimentally link DNA damage and organismal aging: longevity-regulating genetic pathways respond to the accumulation of DNA damage and other stress conditions and conversely influence the rate of damage accumulation and its impact for cancer and aging. This novel insight has emerged from studies on human progeroid diseases and mouse models that have deficient DNA repair pathways. Here we discuss a unified concept of an evolutionarily conserved 'survival' response that shifts the organism's resources from growth to maintenance as an adaptation to stresses, such as starvation and DNA damage. This shift protects the organism from cancer and promotes healthy aging.

Original language	English
Pages (from-to)	77-85
Number of pages	9
Journal	Trends in Genetics
Volume	24
Issue number	2
DOIs	https://doi.org/10.1016/j.tig.2007.11.004
Publication status	Published - Feb 2008
Externally published	Yes

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title = "Age to survive: DNA damage and aging",

abstract = "Aging represents the progressive functional decline and increased mortality risk common to nearly all metazoans. Recent findings experimentally link DNA damage and organismal aging: longevity-regulating genetic pathways respond to the accumulation of DNA damage and other stress conditions and conversely influence the rate of damage accumulation and its impact for cancer and aging. This novel insight has emerged from studies on human progeroid diseases and mouse models that have deficient DNA repair pathways. Here we discuss a unified concept of an evolutionarily conserved 'survival' response that shifts the organism's resources from growth to maintenance as an adaptation to stresses, such as starvation and DNA damage. This shift protects the organism from cancer and promotes healthy aging.",

author = "Bj{\"o}rn Schumacher and Garinis, {George A.} and Hoeijmakers, {Jan H.J.}",

note = "Funding Information: We apologize for omitting citation of numerous primary papers because of space limitations. We acknowledge funding from SenterNovem IOP-Genomics (IGE03009), National Institutes of Health (1PO1 AG17242), Netherlands Organization for Scientific Research (NWO) and EC (Integrated project DNA repair). B.S. is supported by EMBO long-term, Marie Curie Intra-European fellowships and a Veni grant of the Netherlands Science Organization (NWO), and G.G. is supported by the Cancer Genomics Centre.",

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doi = "10.1016/j.tig.2007.11.004",

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AU - Garinis, George A.

AU - Hoeijmakers, Jan H.J.

N1 - Funding Information: We apologize for omitting citation of numerous primary papers because of space limitations. We acknowledge funding from SenterNovem IOP-Genomics (IGE03009), National Institutes of Health (1PO1 AG17242), Netherlands Organization for Scientific Research (NWO) and EC (Integrated project DNA repair). B.S. is supported by EMBO long-term, Marie Curie Intra-European fellowships and a Veni grant of the Netherlands Science Organization (NWO), and G.G. is supported by the Cancer Genomics Centre.

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N2 - Aging represents the progressive functional decline and increased mortality risk common to nearly all metazoans. Recent findings experimentally link DNA damage and organismal aging: longevity-regulating genetic pathways respond to the accumulation of DNA damage and other stress conditions and conversely influence the rate of damage accumulation and its impact for cancer and aging. This novel insight has emerged from studies on human progeroid diseases and mouse models that have deficient DNA repair pathways. Here we discuss a unified concept of an evolutionarily conserved 'survival' response that shifts the organism's resources from growth to maintenance as an adaptation to stresses, such as starvation and DNA damage. This shift protects the organism from cancer and promotes healthy aging.

AB - Aging represents the progressive functional decline and increased mortality risk common to nearly all metazoans. Recent findings experimentally link DNA damage and organismal aging: longevity-regulating genetic pathways respond to the accumulation of DNA damage and other stress conditions and conversely influence the rate of damage accumulation and its impact for cancer and aging. This novel insight has emerged from studies on human progeroid diseases and mouse models that have deficient DNA repair pathways. Here we discuss a unified concept of an evolutionarily conserved 'survival' response that shifts the organism's resources from growth to maintenance as an adaptation to stresses, such as starvation and DNA damage. This shift protects the organism from cancer and promotes healthy aging.

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Age to survive: DNA damage and aging

Abstract

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