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Abstract
Aging is characterized by functional decline of diverse organs and an increased risk for several diseases. Therefore, a high interest exists in understanding the molecular mechanisms that stimulate aging at all levels, from cells and tissues to organs and organisms, in order to develop ways to promote healthy aging. While many molecular and biochemical mechanisms are already understood in some detail, the role of changes in epigenetic regulation has only begun to be considered in recent years. The age-dependent global reduction in heterochromatin, along with site-specific changes in the patterns of DNA methylation and modification of histones, have been observed in several aging model systems. However, understanding of the precise role of such changes requires further research. In this review, we will discuss the role of epigenetic regulation in aging and indicate future research directions that will help elucidate the mechanistic details of it.
Highlights
Aging is an associated with an increased risk of several morbidities such cancer, cardiovascular disease, and autoimmune disease
The analysis of additional time points around the onset of thymic involution may help in determining cell type and the stage of thymus development in which the downregulation of SUV39H1 and DNMT1 occurs. If it occurs relatively early, this may suggest that the associated heterochromatin loss, genomic instability, and alterations in the gene expression profile may play a causal role in the induction of senescence and/or apoptosis in the affected cell types
If the downregulation of SUV39H1 and DNMT1 does occur relatively early during thymic involution, it would be interesting to further study their role in the onset of thymic involution by creating mouse-models that overexpress or repress SUV39H1 or DNMT1 in the thymus or possibly even in a specific cell type that is affected by their age-dependent downregulation (Sidler et al, 2013)
Summary
Aging is an associated with an increased risk of several morbidities such cancer, cardiovascular disease, and autoimmune disease. Aging is associated with a loss of heterochromatin marks, including H3K9me3 with corresponding reduction in SUV39H1 expression and increased genomic instability in the thymus (Sidler et al, 2013). The shift to hypomethylation of constitutive heterochromatin and hypermethylation of promoters in cell-cycle promoting genes, age-dependent changes in DNA methylation may trigger increased genomic instability and lead to a permanent cell-cycle arrest.
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