Aging and genome maintenance: lessons from the mouse?
Recent progress in the science of aging is driven largely by the use of model systems, ranging from yeast and nematodes to mice. These models have revealed conservation in genetic pathways that balance energy production and its damaging by-products with pathways that preserve somatic maintenance. Maintaining genome integrity has emerged as a major factor in longevity and cell viability. Here we discuss the use of mouse models with defects in genome maintenance for understanding the molecular basis of aging in humans.
Hasty
Paul
P
Department of Molecular Medicine, University of Texas Health Science Center, San Antonio, TX 78245, USA. hastye@uthscsa.edu
Campisi
Judith
J
Hoeijmakers
Jan
J
van Steeg
Harry
H
Vijg
Jan
J
D000375:Aging / Q000235:genetics; D019588:Aging, Premature / Q000235:genetics*; D000818:Animals; D017209:Apoptosis; D016922:Cellular Senescence; D004249:DNA Damage; D004265:DNA Helicases / Q000235:genetics / Q000378:metabolism; D004260:DNA Repair / Q000235:genetics; D005090:Exodeoxyribonucleases; D016678:Genome; D015894:Genome, Human; D006801:Humans; D008136:Longevity / Q000235:genetics; D051379:Mice; D009154:Mutation; D017382:Reactive Oxygen Species / Q000378:metabolism; D053484:RecQ Helicases; D013577:Syndrome; D016615:Telomere / Q000502:physiology; D014158:Transcription, Genetic; D000071657:Werner Syndrome Helicase
D017382:Reactive Oxygen Species; D005090:Exodeoxyribonucleases; D004265:DNA Helicases; D053484:RecQ Helicases; C098785:WRN protein, human; D000071657:Werner Syndrome Helicase