The Role of Iron, Its Metabolism and Ferroptosis in Traumatic Brain Injury.

The Role of Iron, Its Metabolism and Ferroptosis in Traumatic Brain Injury.
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铁的作用、其代谢和铁死亡在创伤性脑损伤中的作用。

DOI:
10.3389/fncel.2020.590789
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发表时间:
2020
影响因子:
5.3
通讯作者:
He Y
He Y
中科院分区:
医学2区
文献类型:
--
作者:
Tang S;Gao P;Chen H;Zhou X;Ou Y;He Y

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Traumatic brain injury (TBI) is a structural and physiological disruption of brain function caused by external forces. It is a major cause of death and disability for patients worldwide. TBI includes both primary and secondary impairments. Iron overload and ferroptosis highly involved in the pathophysiological process of secondary brain injury. Ferroptosis is a form of regulatory cell death, as increased iron accumulation in the brain leads to lipid peroxidation, reactive oxygen species (ROS) production, mitochondrial dysfunction and neuroinflammatory responses, resulting in cellular and neuronal damage. For this reason, eliminating factors like iron deposition and inhibiting lipid peroxidation may be a promising therapy. Iron chelators can be used to eliminate excess iron and to alleviate some of the clinical manifestations of TBI. In this review we will focus on the mechanisms of iron and ferroptosis involving the manifestations of TBI, broaden our understanding of the use of iron chelators for TBI. Through this review, we were able to better find novel clinical therapeutic directions for further TBI study.
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