The effect of Ferroptosis -related Mitochondrial Dysfunction in the Development of Temporal Lobe Epilepsy

癫痫 颞叶 神经科学 机制(生物学) 氧化应激 发病机制 线粒体 生物 细胞生物学 免疫学 内分泌学 哲学 认识论
作者
Yang Su,Ningrui Cao,Dingkun Zhang,Minjin Wang
出处
期刊:Ageing Research Reviews [Elsevier BV]
卷期号:96: 102248-102248 被引量:8
标识
DOI:10.1016/j.arr.2024.102248
摘要

Temporal lobe epilepsy (TLE) is the most common form of epileptic syndrome. It has been established that due to its complex pathogenesis, a considerable proportion of TLE patients often progress to drug-resistant epilepsy. Ferroptosis has emerged as an important neuronal death mechanism in TLE, which is primarily influenced by lipid accumulation and oxidative stress. In previous studies of ferroptosis, more attention has been focused on the impact of changes in the levels of proteins related to the redox equilibrium and signaling pathways on epileptic seizures. However, it is worth noting that the oxidative-reduction changes in different organelles may have different pathophysiological significance in the process of ferroptosis-related diseases. Mitochondria, as a key organelle involved in ferroptosis, its structural damage and functional impairment can lead to energy metabolism disorders and disruption of the excitatory inhibitory balance, significantly increasing the susceptibility to epileptic seizures. Therefore, secondary mitochondrial dysfunction in the process of ferroptosis could play a crucial role in TLE pathogenesis. This review focuses on ferroptosis and mitochondria, discussing the pathogenic role of ferroptosis-related mitochondrial dysfunction in TLE, thus aiming to provide novel insights and potential implications of ferroptosis-related secondary mitochondrial dysfunction in epileptic seizures and to offer new insights for the precise exploration of ferroptosis-related therapeutic targets for TLE patients.
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