Metabolism, ubiquinone synthesis, and longevity

Abstract

Until recently, the mechanisms that control the aging process were thought to be immensely complex and nearly impossible to dissect at the molecular level. However, genetic analysis, primarily in model organisms such as yeast, worms, and flies, is dramatically changing this view. It seems that at least three distinct genetic networks control the aging process. These networks include the insulin/IGF-1 signaling pathway, signaling that arises from the mitochondrial electron transport chain, and finally, mechanisms that govern the response to dietary restriction. The use of invertebrates as model organisms to study aging has been extensive, since the ease of genetic manipulation and short life span give them desirable characteristics. However, the question often remains as to whether we can draw the same conclusions in higher organisms. Some of the life-lengthening pathways discovered in invertebrates (i.e., knocking down insulin/IGF-1 signaling) are conserved in mammals; however, distinguishing between species-specific models of aging and universal processes remains a major challenge in the field. Indeed, the conservation of such processes is key to the validation of the use of model organisms to study the aging process. Hekimi and colleagues (Liu et al. 2005) in this issue of Genes and Development substantiates the use of the round worm, Caenorhabditis elegans, as an excellent model for the study of the role of mitochondria in the aging process of mammals.