Mitochondrial iron homeostasis and its dysfunctions in neurodegenerative disorders
Author
dc.contributor.author
Mena, Natalia P.
Author
dc.contributor.author
Urrutia, Pamela J.
Author
dc.contributor.author
Lourido, Fernanda
Author
dc.contributor.author
Carrasco, Carlos M.
Author
dc.contributor.author
Núñez González, Marco
Admission date
dc.date.accessioned
2015-07-30T16:07:08Z
Available date
dc.date.available
2015-07-30T16:07:08Z
Publication date
dc.date.issued
2015
Cita de ítem
dc.identifier.citation
Mitochondrion 21 (2015) 92–105
en_US
Identifier
dc.identifier.other
DOI: 10.1016/j.mito.2015.02.001
Identifier
dc.identifier.uri
https://repositorio.uchile.cl/handle/2250/132259
General note
dc.description
Artículo de publicación ISI
en_US
Abstract
dc.description.abstract
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 fromelectrons
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.
en_US
Patrocinador
dc.description.sponsorship
National Council for Scientific and Technological Research of Chile: FONDECYT
1130068
Program of Associative Research
ACT1114
CONICYT
3654593