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DNA repair, genome stability, and aging

David B Lombard1, Katrin F Chua, Raul Mostoslavsky

  • 1Howard Hughes Medical Institute, The Children's Hospital, Department of Genetics, Harvard Medical School and, The CBR Institute for Biomedical Research, Boston, Massachusetts 02115, USA.

Cell
|March 1, 2005
PubMed

Insights

Aging is linked to DNA damage accumulation and impaired DNA repair, which can accelerate aging processes. This review explores the connection between genomic instability and aging, highlighting cellular responses and future research directions.

Area of Science:

  • Gerontology
  • Molecular Biology
  • Genetics

Background:

  • Aging is characterized by functional decline and increased mortality.
  • Accumulation of nuclear DNA lesions is a hallmark of the aging process.
  • Defects in DNA repair mechanisms can lead to premature aging phenotypes.

Purpose of the Study:

  • To review the evidence linking aging to nuclear DNA lesions.
  • To discuss the role of cellular DNA damage responses in aging manifestations.
  • To explore the function of Sir2 in genomic stability, metabolism, and aging.

Main Methods:

  • Literature review of aging research.
  • Analysis of studies on DNA damage and repair in aging.
  • Examination of the role of Sir2 and mutant mouse models.

Main Results:

  • DNA damage increases with age.
  • Impaired DNA repair is associated with premature aging.
  • Cellular DNA damage responses contribute to aging.
  • Sir2 links genomic stability, metabolism, and aging.

Conclusions:

  • Genomic instability, particularly DNA damage, is a key factor in aging.
  • Cellular responses to DNA damage play a significant role in aging.
  • Mutant mice are valuable tools for aging research, with further investigation needed.

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