Mitochondrial iron metabolism and neurodegenerative diseases

被引:44
|
作者
Cheng, Ruiying [1 ]
Dhorajia, Varun V. [2 ]
Kim, Jonghan [1 ]
Kim, Yuho [3 ]
机构
[1] Univ Massachusetts Lowell, Dept Biomed & Nutr Sci, Lowell, MA 01854 USA
[2] UMass Biomed Engn & Biotechnol, Lowell, MA USA
[3] Univ Massachusetts Lowell, Dept Phys Therapy & Kinesiol, Lowell, MA 01854 USA
关键词
Brain iron; Iron overload; Iron transport; Mitochondria; Neuron; FRATAXIN DEFICIENCY LEADS; METAL TRANSPORTER 1; TARGETING A-BETA; BRAIN IRON; HUNTINGTONS-DISEASE; OXIDATIVE STRESS; FRIEDREICHS-ATAXIA; SULFUR CLUSTER; PARKINSONS-DISEASE; FERRITIN ACCUMULATION;
D O I
10.1016/j.neuro.2021.11.003
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Iron is a key element for mitochondrial function and homeostasis, which is also crucial for maintaining the neuronal system, but too much iron promotes oxidative stress. A large body of evidence has indicated that abnormal iron accumulation in the brain is associated with various neurodegenerative diseases such as Huntington's disease, Alzheimer's disease, Parkinson's disease, and Friedreich's ataxia. However, it is still unclear how irregular iron status contributes to the development of neuronal disorders. Hence, the current review provides an update on the causal effects of iron overload in the development and progression of neurodegenerative diseases and discusses important roles of mitochondrial iron homeostasis in these disease conditions. Furthermore, this review discusses potential therapeutic targets for the treatments of iron overload-linked neurodegenerative diseases.
引用
收藏
页码:88 / 101
页数:14
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