The process of aging involves the accumulating changes in the microenvironment that lead to cell senescence or apoptosis, and subsequent tissue or organ dysfunction. Multiple extrinsic and intrinsic events that cause
DNA instability are associated with aging. Cells containing unstable
DNA are biologically vulnerable, and if the DNA damage is too great for the cell to repair, it becomes senescent or dies by apoptosis. Thus, the cell's capacity to repair its
DNA determines the progress of aging, at least in part. Here, we focus on the
sirtuins, the mammalian homologs of the yeast life-span-extending molecule, Sir2. Among the
sirtuin family
proteins in mammals, the one most similar to yeast Sir2 is
SIRT1, which is involved in multiple pathways, including the repair of
DNA double-strand breaks. Although the role of
SIRT1 in mammalian longevity is not clear, it is expressed throughout the retina, where it may suppress aging. In fact, a mutant mouse model of
retinal degeneration shows an abnormal subcellular localization of
SIRT1 protein and accelerated
retinal cell apoptosis. Further analyses are required to elucidate the mechanism of DNA damage and repair, including the contributions of the
sirtuins, in the aged or diseased retinas, which will help us understand the mechanisms of
retinal aging.