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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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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1612058933212479488 |