Nuclear and mitochondrial DNA repair in selected eukaryotic aging model systems.
Knowledge about the different mechanisms underlying the aging process has increased exponentially in the last decades. The fact that the basic mechanisms involved in the aging process are believed to be universal allows the use of different model systems, from the simplest eukaryotic cells such as fungi to the most complex organisms such as mice or human. As our knowledge on the aging mechanisms in those model systems increases, our understanding of human aging and the potential interventions that we could approach rise significantly. Among the different mechanisms that have been implicated in the aging process, DNA repair is one of the processes which have been suggested to play an important role. Here, we review the latest investigations supporting the role of these mechanisms in the aging process, stressing how beneficial the use of different model systems is. We discuss how human genetic studies as well as several investigations on mammalian models and simpler eukaryotic organisms have contributed to a better understanding of the involvement of DNA repair mechanisms in aging.
Department of Physiology, Faculty of Medicine, The Complutense University, Madrid, Spain.
Ricardo
R
Gredilla
Christian
C
Garm
Tinna
T
Stevnsner
D000375:Aging; D019588:Aging, Premature / Q000378:metabolism / Q000473:pathology; D000818:Animals; D002467:Cell Nucleus / Q000378:metabolism*; D004247:DNA / Q000378:metabolism; D059766:DNA End-Joining Repair; D053843:DNA Mismatch Repair; D004260:DNA Repair; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D008954:Models, Biological; D059767:Recombinational DNA Repair
D004247:DNA