Implications of altered iron homeostasis for age-related macular degeneration

Abstract

Reactive oxygen species (ROS) may contribute to the pathogenesis of age-related macular degeneration (AMD) and they can be produced in the Fenton reaction catalyzed by Fe3+ ions. Therefore, altered homeostasis of iron in the retina may be the source of ROS and its damage resulting in clinically detectable AMD symptoms. The results of some post mortem research indicate a higher concentration of iron in AMD retinas in comparison with non-affected retinas, although those results do not determine whether iron overload is the reason or a consequence of AMD. However, the results of some other research suggest that iron may contribute to the pathogenesis of AMD. Those include increasing of macular iron level with age, involvement of iron in the pathogenesis of some degenerative diseases linked with AMD, upregulation of transferrin in AMD, developing of AMD-like syndromes in mice deficient in ceruloplasmin and hephaestin, association between polymorphism of the iron homeostasis genes and AMD and others. Better understanding of the role of altered iron homeostasis may be useful in prevention and curing of AMD.