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Contributions of DNA interstrand cross-links to aging of cells and organisms

Johannes Grillari1, Hermann Katinger, Regina Voglauer

  • 1Institute of Applied Microbiology, Department of Biotechnology, BOKU - University of Natural Resources and Applied Life Sciences, Vienna, Muthgasse 18 1190 Vienna, Austria. Johannes.grillari@boku.ac.at

Nucleic Acids Research
|December 18, 2007
PubMed

Insights

DNA repair pathways, particularly interstrand cross-link (ICL) repair, are implicated in aging. Deficiencies in ICL repair factors contribute to premature aging syndromes and reduced cellular lifespan.

Area of Science:

  • Genetics
  • Molecular Biology
  • Aging Research

Background:

  • DNA damage repair is crucial for maintaining genomic stability and preventing premature aging.
  • Deficiencies in nucleotide excision repair are linked to progeroid syndromes.
  • Emerging evidence suggests a role for interstrand cross-link (ICL) repair in aging.

Purpose of the Study:

  • To review and discuss the potential contribution of interstrand cross-link (ICL) repair to aging.
  • To explore the link between ICL repair defects and progeroid syndromes.
  • To evaluate the impact of ICL-inducing agents on aging phenotypes.

Main Methods:

  • Literature review and synthesis of existing research findings.
  • Analysis of data from human patients and animal models with DNA repair defects.
  • Examination of the long-term effects of ICL-inducing therapies.

Main Results:

  • Systemic administration of DNA cross-linking chemotherapy can induce premature frailty.
  • 8-methoxypsoralen/UVA phototherapy, an ICL-inducing treatment, causes premature skin aging.
  • Mutations in ICL repair factors (e.g., ERCC1/XPF, Fanconi anaemia proteins, WRN) lead to reduced cellular lifespan and progeroid syndromes.

Conclusions:

  • Interstrand cross-link (ICL) repair pathway defects are associated with premature aging and progeroid syndromes.
  • ICL-inducing agents and mutations in ICL repair factors highlight the link between ICL repair and aging.
  • Further research is needed to fully elucidate the specific role of ICL damage in the aging process.

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