Nucleotide excision repair deficiencies and the somatotropic axis in aging

Hormones (Athens). 2008 Jan-Mar;7(1):9-16. doi: 10.14310/horm.2002.1111032.


The physicochemical constitution of DNA cannot warrant lifelong stability. Yet, unlike all other macromolecules, nuclear DNA must last the lifetime of a cell ensuring that its vital genetic information is preserved and faithfully transmitted to progeny. An increasing body of evidence suggests that progressive genome instability likely contributes to aging and shortens lifespan. In support, defects in genome surveillance pathways rapidly accelerate the onset of age-related pathology, including cancer. This review describes the role of DNA damage in aging along with a number of progeroid syndromes and associated mouse models with defects in nucleotide excision repair that age rapidly and die prematurely.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Aging / physiology*
  • Animals
  • DNA / chemistry*
  • DNA Repair / physiology*
  • Disease Models, Animal
  • Human Growth Hormone / genetics*
  • Human Growth Hormone / physiology*
  • Humans
  • Insulin-Like Growth Factor I / genetics
  • Insulin-Like Growth Factor I / physiology
  • Mice


  • Human Growth Hormone
  • Insulin-Like Growth Factor I
  • DNA