Abstract
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.
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Duan, G., Li, J., Duan, Y., Zheng, C., Guo, Q., Li, F., … Long, C. (2023, January 1). Mitochondrial Iron Metabolism: The Crucial Actors in Diseases. Molecules. MDPI. https://doi.org/10.3390/molecules28010029
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