Abstract
Recent studies show that cellular and mitochondrial iron increases with age. Iron overload, especially in mitochondria, increases the availability of redox-active iron, which may be a causal factor in the extensive age-related biomolecular oxidative damage observed in aged organisms. Such damage is thought to play a major role in the pathogenesis of iron overload diseases and age-related pathologies. Indeed, recent findings of the beneficial effects of iron manipulation in life extension in Caenorhabditis elegans, Drosophila and transgenic mice have sparked a renewed interest in the potential role of iron in longevity. A substantial research effort now focuses on developing and testing safe pharmacologic interventions to combat iron dyshomeostasis in aging, acute injuries and in iron overload disorders.