[Relation between genetic and epigenetic mechanisms in aging].

Abstract

The recent identification of genes involved in the regulation of the longevity of some invertebrates (drosophila, nematodes) as well as the presence of human genes exhibiting homologies to those identified in invertebrates, revived the deterministic theories of aging. It appears however that those mechanisms which were shown experimentally to be involved in aging in vertebrates and in particular in humans belong to the epigenetic mechanisms such as the Maillard reaction and free radical attack in particular. Some diseases which imitate an accelerated aging as Progeria and the Werner syndrome are due to mutations, some of them mutagenic themselves. Reflections based on such arguments concerning reactions with catalysers coded in the genome but with activities escaping strict control, suggest an indirect determinism of phenomena involved directly in cell- and tissue aging. These considerations are illustrated by the example of the elastin-laminin receptor studied in our laboratory. Its sustained activation by circulating elastin peptides appears to be involved in cell and tissue aging.