Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases

Mitochondrial ferritin (FtMt) is a novel iron-storage protein in mitochondria. Evidences have shown that FtMt is structurally and functionally similar to the cytosolic H-chain ferritin. It protects mitochondria from iron-induced oxidative damage presumably through sequestration of potentially harmfu...

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Main Authors: Gao, Guofen, Chang, Yan-Zhong
Format: Online
Language:English
Published: Frontiers Media S.A. 2014
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925988/
id pubmed-3925988
recordtype oai_dc
spelling pubmed-39259882014-03-04 Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases Gao, Guofen Chang, Yan-Zhong Pharmacology Mitochondrial ferritin (FtMt) is a novel iron-storage protein in mitochondria. Evidences have shown that FtMt is structurally and functionally similar to the cytosolic H-chain ferritin. It protects mitochondria from iron-induced oxidative damage presumably through sequestration of potentially harmful excess free iron. It also participates in the regulation of iron distribution between cytosol and mitochondrial contents. Unlike the ubiquitously expressed H-ferritin, FtMt is mainly expressed in testis and brain, which suggests its tissue-related roles. FtMt is involved in pathogenesis of neurodegenerative diseases, as its increased expression has been observed in Alzheimer’s disease, restless legs syndrome and Friedreich’s ataxia. Studies from our laboratory showed that in Alzheimer’s disease, FtMt overexpression attenuated the β-amyloid induced neurotoxicity, which on the other hand increased significantly when FtMt expression was knocked down. It is also found that, by maintaining mitochondrial iron homeostasis, FtMt could prevent 6-hydroxydopamine induced dopaminergic cell damage in Parkinson’s disease. These recent findings on FtMt regarding its functions in regulation of brain iron homeostasis and its protective role in pathogenesis of neurodegenerative diseases are summarized and reviewed. Frontiers Media S.A. 2014-02-17 /pmc/articles/PMC3925988/ /pubmed/24596558 http://dx.doi.org/10.3389/fphar.2014.00019 Text en Copyright © 2014 Gao and Chang. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Gao, Guofen
Chang, Yan-Zhong
spellingShingle Gao, Guofen
Chang, Yan-Zhong
Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
author_facet Gao, Guofen
Chang, Yan-Zhong
author_sort Gao, Guofen
title Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
title_short Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
title_full Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
title_fullStr Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
title_full_unstemmed Mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
title_sort mitochondrial ferritin in the regulation of brain iron homeostasis and neurodegenerative diseases
description Mitochondrial ferritin (FtMt) is a novel iron-storage protein in mitochondria. Evidences have shown that FtMt is structurally and functionally similar to the cytosolic H-chain ferritin. It protects mitochondria from iron-induced oxidative damage presumably through sequestration of potentially harmful excess free iron. It also participates in the regulation of iron distribution between cytosol and mitochondrial contents. Unlike the ubiquitously expressed H-ferritin, FtMt is mainly expressed in testis and brain, which suggests its tissue-related roles. FtMt is involved in pathogenesis of neurodegenerative diseases, as its increased expression has been observed in Alzheimer’s disease, restless legs syndrome and Friedreich’s ataxia. Studies from our laboratory showed that in Alzheimer’s disease, FtMt overexpression attenuated the β-amyloid induced neurotoxicity, which on the other hand increased significantly when FtMt expression was knocked down. It is also found that, by maintaining mitochondrial iron homeostasis, FtMt could prevent 6-hydroxydopamine induced dopaminergic cell damage in Parkinson’s disease. These recent findings on FtMt regarding its functions in regulation of brain iron homeostasis and its protective role in pathogenesis of neurodegenerative diseases are summarized and reviewed.
publisher Frontiers Media S.A.
publishDate 2014
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3925988/
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