Mechanisms for Countering Oxidative Stress and Damage in Retinal Pigment Epithelium

Scott M. Plafker, Gary B. O'Mealey, Luke I. Szweda

Research output: Contribution to journalArticlepeer-review

93 Scopus citations


Clinical and experimental evidence supports that chronic oxidative stress is a primary contributing factor to numerous retinal degenerative diseases, such as age-related macular degeneration (AMD). Eyes obtained postmortem from AMD patients have extensive free radical damage to the proteins, lipids, DNA, and mitochondria of their retinal pigment epithelial (RPE) cells. In addition, several mouse models of chronic oxidative stress develop many of the pathological hallmarks of AMD. However, the extent to which oxidative stress is an etiologic component versus its involvement in disease progression remains a major unanswered question. Further, whether the primary target of oxidative stress and damage is photoreceptors or RPE cells, or both, is still unclear. In this review, we discuss the major functions of RPE cells with an emphasis on the oxidative challenges these cells encounter and the endogenous antioxidant mechanisms employed to neutralize the deleterious effects that such stresses can elicit if left unchecked.

Original languageEnglish (US)
Pages (from-to)135-177
Number of pages43
JournalInternational Review of Cell and Molecular Biology
StatePublished - Aug 14 2012


  • Age-related macular degeneration
  • Mitochondria
  • Nrf2
  • Oxidative stress
  • Retinal pigment epithelium
  • Ubiquitin proteolytic system

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology
  • Biochemistry


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