Heterochromatin: an epigenetic point of view in aging

Aging: changes in genome infrastructure Biochemical pathways that alter the physical organization of the genome could play a prominent role in age-related cellular degeneration. Chromosomal DNA is wound around proteins known as histones; when such assemblies are packed closely together, the genes in compacted regions are generally silenced. Jong-Hyuk Lee, Vilhelm A. Bohr and colleagues at the US National Institutes of Health, Baltimore, have reviewed evidence linking these 'heterochromatin' regions of the genome to the aging process. They find that diseases associated with premature age-related tissue degeneration are frequently marked by abnormal activity in genes involved in heterochromatin remodeling. Several biochemical and genetic factors that have been shown to experimentally reverse biological aging in experimental settings also appear to affect heterochromatin remodeling. Closer examination of the relevant remodeling processes could therefore reveal fundamental biological drivers of age-related degeneration. Aging is an inevitable process of life. Defined by progressive physiological and functional loss of tissues and organs, aging increases the risk of mortality for the organism. The aging process is affected by various factors, including genetic and epigenetic ones. Here, we review the chromatin-specific epigenetic changes that occur during normal (chronological) aging and in premature aging diseases. Taking advantage of the reversible nature of epigenetic modifications, we will also discuss possible lifespan expansion strategies through epigenetic modulation, which was considered irreversible until recently.