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The emerging role of iron dyshomeostasis in the mitochondrial decay of aging Xu J; Marzetti E; Seo AY; Kim JS; Prolla TA; Leeuwenburgh CMech Ageing Dev 2010[Jul]; 131 (7-8): 487-93Recent 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.|Age Factors[MESH]|Aging/*metabolism[MESH]|Animals[MESH]|Cellular Senescence[MESH]|Homeostasis[MESH]|Humans[MESH]|Iron Overload/*metabolism[MESH]|Iron/*metabolism[MESH]|Longevity[MESH]|Mitochondria/*metabolism[MESH]|Mitochondrial Diseases/*metabolism[MESH]|Oxidation-Reduction[MESH]|Oxidative Stress[MESH]|Reactive Oxygen Species/metabolism[MESH] |
