The emerging role of iron dyshomeostasis in the mitochondrial decay of aging

Jinze Xu, Emanuele Marzetti, Arnold Y. Seo, Jae Sung Kim, Tomas A. Prolla, Christiaan Leeuwenburgh

Research output: Contribution to journalArticle

41 Scopus citations

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.

Original languageEnglish
Pages (from-to)487-493
Number of pages7
JournalMechanisms of Ageing and Development
Volume131
Issue number7-8
DOIs
StatePublished - Jul 1 2010
Externally publishedYes

Keywords

  • Aging
  • Iron accumulation
  • Iron overload
  • Labile iron
  • Mitochondrial dysfunction

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