RPE cell senescence: a key contributor to age-related macular degeneration

Med Hypotheses. 2012 Apr;78(4):505-10. doi: 10.1016/j.mehy.2012.01.018. Epub 2012 Jan 30.


Age-related macular degeneration (AMD) is the leading cause of blindness in industrialized countries. Although much progress has been made recently in the management of later stages of the disease, no agents have yet been developed for the early stages or for prophylactic use. Furthermore, even the treatments for the later stages have limited effectiveness. The process of developing improved treatments for AMD is complicated by the existence of several theories concerning the cause of the disorder, each suggesting a different strategy for finding effective therapeutics. One of the potential contributors to AMD pathology is retinal pigment epithelial (RPE) cell senescence. The present paper hypothesizes that RPE senescence plays a central role in the etiology of AMD. This hypothesis is supported by the ability of RPE cell senescence to account for the signs, risk factors, and successful treatment modalities of the disorder. This hypothesis also points to several new prophylactic and treatment strategies for AMD.

MeSH terms

  • Cellular Senescence / physiology*
  • Choroidal Neovascularization / physiopathology
  • Complement Factor H / genetics
  • DEAD-box RNA Helicases / metabolism
  • Estrogens / pharmacology
  • Fatty Acids, Omega-3 / pharmacology*
  • Geographic Atrophy / physiopathology
  • Humans
  • Macular Degeneration / etiology*
  • Macular Degeneration / pathology*
  • Retinal Drusen / physiopathology
  • Retinal Pigment Epithelium / cytology*
  • Ribonuclease III / metabolism
  • Risk Factors
  • Vitamin D / pharmacology


  • Estrogens
  • Fatty Acids, Omega-3
  • Vitamin D
  • Complement Factor H
  • DICER1 protein, human
  • Ribonuclease III
  • DEAD-box RNA Helicases