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中国临床药理学与治疗学 ›› 2025, Vol. 30 ›› Issue (6): 828-834.doi: 10.12092/j.issn.1009-2501.2025.06.013

• 综述与讲座 • 上一篇    下一篇

靶向铁死亡与癫痫治疗研究进展

赵亚红,李强   

  1. 赤峰学院附属医院神经内科,赤峰  024005,内蒙古
  • 收稿日期:2024-06-24 修回日期:2024-07-20 出版日期:2025-06-26 发布日期:2025-06-09
  • 通讯作者: 李强,男,硕士,主任医师,硕士研究生导师,研究方向:神经变性病发病机制临床与基础工作。 E-mail: liqiang1980_1981@126.com
  • 作者简介:赵亚红,女,硕士,副主任医师,研究方向:癫痫发病机制与防治。 E-mail: 1056250229@qq.com
  • 基金资助:
    内蒙古自然科学基金项(2022MS08046);赤峰市自然基金项目(SZR2023053);内蒙古人类遗传病研究自治区高等学校重点实验室开放课题(YC202305,YC202304);内蒙古自治区硕士研究生科学创新项目(S20231204Z)

Targeting ferroptosis offers a novel therapeutic approaches in epilepsy

ZHAO Yahong, LI Qiang    

  1. Department of Neurology, The Affiliated Hospital of Chifeng University, Chifeng 024005, Inner Mongolia, China
  • Received:2024-06-24 Revised:2024-07-20 Online:2025-06-26 Published:2025-06-09

摘要:

癫痫是由大脑神经元异常放电引起的突然、反复和短暂的中枢神经系统功能障碍。反复发作或长时间癫痫发作可导致神经元损伤和细胞死亡;然而,癫痫对神经元损伤的分子机制尚不清楚。铁死亡是一种新型的调节性细胞死亡,其特征是铁依赖性脂质过氧化,与癫痫的病理生理进展有关。研究表明,药理学上抑制铁死亡可以减轻癫痫导致的神经元损伤。本文简要描述了铁死亡的核心分子机制及其在癫痫发病中的作用,重点介绍了能够通过抑制铁死亡治疗癫痫药物的现状和作用机制。

关键词: 癫痫, 铁死亡, 铁死亡抑制剂, 神经保护

Abstract:

Epilepsy is sudden, recurrent, and transient central nervous system dysfunction caused by abnormal discharge of neurons in the brain. Recurrent or prolonged seizures can result in neuronal damage and cell death; however, the molecular mechanisms underlying the epilepsy-induced damage to neurons remain unclear. Ferroptosis, a novel type of regulated cell death (RCD) characterized by iron-dependent lipid peroxidation, is involved in the pathophysiological progression of epilepsy. Emerging studies have demonstrated pharmacologically inhibiting ferroptosis can mitigate neuronal damage in epilepsy. In this review, we briefly describe the core molecular mechanisms of ferroptosis and the roles they play in contributing to epilepsy, highlight emerging compounds that can inhibit ferroptosis to treat epilepsy and associated neurobehavioral comorbidities, and outline their pharmacological beneficial effects. The current review suggests inhibiting ferroptosis as a therapeutic target for epilepsy and associated neurobehavioral comorbidities.

Key words: epilepsy, ferroptosis, ferroptosis inhibitors, neuroprotection

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