Retinal aging and sirtuins

Yoko Ozawa, Shunsuke Kubota, Toshio Narimatsu, Kenya Yuki, Takashi Koto, Mariko Sasaki, Kazuo Tsubota

Research output: Contribution to journalReview articlepeer-review

24 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)199-203
Number of pages5
JournalOphthalmic research
Volume44
Issue number3
DOIs
Publication statusPublished - 2010 Sep

Keywords

  • Apoptosis
  • Cell senescence
  • Retinal aging
  • Sirtuin

ASJC Scopus subject areas

  • Ophthalmology
  • Sensory Systems
  • Cellular and Molecular Neuroscience

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