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Mitochondrial Iron Metabolism: The Crucial Actors in Diseases
Iron is a trace element necessary for cell growth, development, and cellular homeostasis, but insufficient or excessive level of iron is toxic. Intracellularly, sufficient amounts of iron are required for mitochondria (the center of iron utilization) to maintain their normal physiologic function. Ir...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9822237/ https://www.ncbi.nlm.nih.gov/pubmed/36615225 http://dx.doi.org/10.3390/molecules28010029 |
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author | Duan, Geyan Li, Jianjun Duan, Yehui Zheng, Changbing Guo, Qiuping Li, Fengna Zheng, Jie Yu, Jiayi Zhang, Peiwen Wan, Mengliao Long, Cimin |
author_facet | Duan, Geyan Li, Jianjun Duan, Yehui Zheng, Changbing Guo, Qiuping Li, Fengna Zheng, Jie Yu, Jiayi Zhang, Peiwen Wan, Mengliao Long, Cimin |
author_sort | Duan, Geyan |
collection | PubMed |
description | Iron is a trace element necessary for cell growth, development, and cellular homeostasis, but insufficient or excessive level of iron is toxic. Intracellularly, sufficient amounts of iron are required for mitochondria (the center of iron utilization) to maintain their normal physiologic function. Iron deficiency impairs mitochondrial metabolism and respiratory activity, while mitochondrial iron overload promotes ROS production during mitochondrial electron transport, thus promoting potential disease development. This review provides an overview of iron homeostasis, mitochondrial iron metabolism, and how mitochondrial iron imbalances-induced mitochondrial dysfunction contribute to diseases. |
format | Online Article Text |
id | pubmed-9822237 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-98222372023-01-07 Mitochondrial Iron Metabolism: The Crucial Actors in Diseases Duan, Geyan Li, Jianjun Duan, Yehui Zheng, Changbing Guo, Qiuping Li, Fengna Zheng, Jie Yu, Jiayi Zhang, Peiwen Wan, Mengliao Long, Cimin Molecules Review Iron is a trace element necessary for cell growth, development, and cellular homeostasis, but insufficient or excessive level of iron is toxic. Intracellularly, sufficient amounts of iron are required for mitochondria (the center of iron utilization) to maintain their normal physiologic function. Iron deficiency impairs mitochondrial metabolism and respiratory activity, while mitochondrial iron overload promotes ROS production during mitochondrial electron transport, thus promoting potential disease development. This review provides an overview of iron homeostasis, mitochondrial iron metabolism, and how mitochondrial iron imbalances-induced mitochondrial dysfunction contribute to diseases. MDPI 2022-12-21 /pmc/articles/PMC9822237/ /pubmed/36615225 http://dx.doi.org/10.3390/molecules28010029 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Duan, Geyan Li, Jianjun Duan, Yehui Zheng, Changbing Guo, Qiuping Li, Fengna Zheng, Jie Yu, Jiayi Zhang, Peiwen Wan, Mengliao Long, Cimin Mitochondrial Iron Metabolism: The Crucial Actors in Diseases |
title | Mitochondrial Iron Metabolism: The Crucial Actors in Diseases |
title_full | Mitochondrial Iron Metabolism: The Crucial Actors in Diseases |
title_fullStr | Mitochondrial Iron Metabolism: The Crucial Actors in Diseases |
title_full_unstemmed | Mitochondrial Iron Metabolism: The Crucial Actors in Diseases |
title_short | Mitochondrial Iron Metabolism: The Crucial Actors in Diseases |
title_sort | mitochondrial iron metabolism: the crucial actors in diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9822237/ https://www.ncbi.nlm.nih.gov/pubmed/36615225 http://dx.doi.org/10.3390/molecules28010029 |
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