Mitophagy and iron: two actors sharing the stage in age-associated neuronal pathologies

Alfonso Schiavi, Flavie Strappazzon, Natascia Ventura

Research output: Contribution to journalArticlepeer-review


Aging is characterized by the deterioration of different cellular and organismal structures and functions. A typical hallmark of the aging process is the accumulation of dysfunctional mitochondria and excess iron, leading to a vicious cycle that promotes cell and tissue damage, which ultimately contribute to organismal aging. Accordingly, altered mitochondrial quality control pathways such as mitochondrial autophagy (mitophagy) as well as altered iron homeostasis, with consequent iron overload, can accelerate the aging process and the development and progression of different age-associated disorders. In this review we first briefly introduce the aging process and summarize molecular mechanisms regulating mitophagy and iron homeostasis. We then provide an overview on how dysfunction of these two processes impact on aging and age-associated neurodegenerative disorders with a focus on Alzheimer's disease, Parkinson's disease and Amyotrophic Lateral Sclerosis. Finally, we summarize some recent evidence showing mechanistic links between iron metabolism and mitophagy and speculate on how regulating the crosstalk between the two processes may provide protective effects against aging and age-associated neuronal pathologies.

Original languageEnglish
Article number111252
JournalMechanisms of Ageing and Development
Publication statusPublished - Jun 2020


  • Aging
  • Alzheimer disease
  • Amyotrophic Lateral Sclerosis
  • Iron
  • Mitochondria
  • Parkinson disease

ASJC Scopus subject areas

  • Ageing
  • Developmental Biology


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