The emerging role of iron dyshomeostasis in the mitochondrial decay of aging.
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.
Xu
Jinze
J
Department of Aging and Geriatrics Research, Division of Biology of Aging, Genomics, Metabolism and Biomarkers Core of the Institute on Aging, University of Florida, Gainesville, FL 32611, USA.
Marzetti
Emanuele
E
Seo
Arnold Y
AY
Kim
Jae-Sung
JS
Prolla
Tomas A
TA
Leeuwenburgh
Christiaan
C
D000367:Age Factors; D000375:Aging / Q000378:metabolism*; D000818:Animals; D016922:Cellular Senescence; D006706:Homeostasis; D006801:Humans; D007501:Iron / Q000378:metabolism*; D019190:Iron Overload / Q000378:metabolism*; D008136:Longevity; D008928:Mitochondria / Q000378:metabolism*; D028361:Mitochondrial Diseases / Q000378:metabolism*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D017382:Reactive Oxygen Species / Q000378:metabolism
D017382:Reactive Oxygen Species; D007501:Iron