Abstract

Epilepsy is a disease characterized by recurrent, episodic, and transient central nervous system (CNS) dysfunction resulting from an excessive synchronous discharge of brain neurons. It is characterized by diverse etiology, complex pathogenesis, and difficult treatment. In addition, most epileptic patients exhibit social cognitive impairment and psychological impairment. Iron is an essential trace element for human growth and development and is also involved in a variety of redox reactions in organisms. However, abnormal iron metabolism is associated with several neurological disorders, including hemorrhagic post-stroke epilepsy and post-traumatic epilepsy (PTE). Moreover, ferroptosis is also considered a new form of regulation of cell death, which is attributed to severe lipid peroxidation caused by the production of reactive oxygen species (ROS) and iron overload found in various neurological diseases, including epilepsy. Therefore, this review summarizes the study on iron metabolism and ferroptosis in epilepsy, in order to elucidate the correlation between iron and epilepsy. It also provides a novel method for the treatment, prevention, and research of epilepsy, to control epileptic seizures and reduce nerve injury after the epileptic seizure.

Highlights

  • Epilepsy is a disease characterized by recurrent, episodic, and transient central nervous system (CNS) dysfunction resulting from an excessive synchronous discharge of brain neurons and both the morbidity and mortality are high

  • The findings revealed that iron in mesial temporal lobe epilepsy (MTLE) Is redistributed between subcortical and cortical structures, and the degree of redistribution is influenced by the progression of epilepsy and precipitation factors (Zhang et al, 2014)

  • Iron chaperone Poly rC binding protein 1 (PCBP1) can limit the toxicity of intracellular iron and prevent Ferroptosis caused by lipid peroxidation SIRT3 deficiency is resistant to autophagy-dependent ferroptosis by inhibiting the AMPK/mTOR pathway and promoting glutathione peroxidase 4 (GPX4) levels Histone demethylase KDM3B protects against ferroptosis by upregulating SLC7A11

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Summary

Introduction

Epilepsy is a disease characterized by recurrent, episodic, and transient CNS dysfunction resulting from an excessive synchronous discharge of brain neurons and both the morbidity and mortality are high. Ferroptosis is a new form of regulated cell death, attributed to severe lipid peroxidation caused by the production of ROS and iron overload and detected in several neurological diseases, including epilepsy (Kahn-Kirby et al, 2019). It is considered a new form of cell death regulation, attributed to severe lipid peroxidation caused by ROS and iron overload and found in a variety of neurological diseases, including epilepsy.

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