Mitochondrial iron homeostasis and its dysfunctions in neurodegenerative disorders
| Autor: | Fernanda Lourido, Pamela J. Urrutia, Marco T. Núñez, Carlos M. Carrasco, Natalia Mena |
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| Rok vydání: | 2015 |
| Předmět: |
Iron-Sulfur Proteins
Programmed cell death Ataxia Iron Iron–sulfur cluster Heme Disease Mitochondrion Biology chemistry.chemical_compound Organelle medicine Animals Homeostasis Humans Molecular Biology Neurons chemistry.chemical_classification Reactive oxygen species Cell Death Neurodegenerative Diseases Cell Biology Mitochondria Cell biology chemistry Biochemistry Molecular Medicine medicine.symptom Reactive Oxygen Species |
| Zdroj: | Mitochondrion. 21:92-105 |
| ISSN: | 1567-7249 |
| DOI: | 10.1016/j.mito.2015.02.001 |
| Popis: | Synthesis of the iron-containing prosthetic groups-heme and iron-sulfur clusters-occurs in mitochondria. The mitochondrion is also an important producer of reactive oxygen species (ROS), which are derived from electrons leaking from the electron transport chain. The coexistence of both ROS and iron in the secluded space of the mitochondrion makes this organelle particularly prone to oxidative damage. Here, we review the elements that configure mitochondrial iron homeostasis and discuss the principles of iron-mediated ROS generation in mitochondria. We also review the evidence for mitochondrial dysfunction and iron accumulation in Alzheimer's disease, Huntington Disease, Friedreich's ataxia, and in particular Parkinson's disease. We postulate that a positive feedback loop of mitochondrial dysfunction, iron accumulation, and ROS production accounts for the process of cell death in various neurodegenerative diseases in which these features are present. |
| Databáze: | OpenAIRE |
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