Nucleotide-excision repair deficiency: Acausative factor for accelerated aging diseases in humans?

Ming Yin, Qingyi Wei

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Nucleotide excision repair (NER) recognizes and removes bulky DNA damage that leads to DNA double-helix distortion. Inherited defects in the NER pathway have been associated with aging symptoms and premature death. In this review, we discussed the mechanisms of how NER maintains genomic integrity and affects clinical outcomes, if NER is compromised, and the role of NER as a potential causative factor for mammalian aging. We summarized current evidence of the association between NER and aging process through a discussion of most updated research findings from genetic models of mice and molecular epidemiological studies from humans. Several possible mechanisms by which NER influences aging are suggested, including the GH/IGF1 axis, p53-induced apoptosis/senescence in response to DNA damage, reactive oxygen species (ROS), and maintenance of telomerase activities. A comparison between normal aging and NER deficiency-related aging is also made to illustrate their similarities and discrepancies. We conclude with a number of issues needed to be resolved to further clarify the relationship between NER and aging process in humans.

Original languageEnglish (US)
Title of host publicationDNA Damage Repair, Repair Mechanisms and Aging
PublisherNova Science Publishers, Inc.
Pages205-222
Number of pages18
ISBN (Print)9781616689148
StatePublished - 2012

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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