摘要
周围神经损伤(PNI)后,铁死亡通过铁依赖性脂质过氧化参与神经细胞损伤和功能障碍。自噬作为一种细胞内降解过程,通过清除受损线粒体、调节铁稳态和抗氧化系统等路径干预铁死亡,进而促进神经修复。特别是线粒体自噬和铁蛋白自噬能够调控铁死亡的发生,成为PNI治疗的潜在靶点。当前关于自噬与铁死亡相互作用机制的研究仍处于起步阶段,未来可进一步聚焦关键自噬因子在铁稳态调控中的作用,探索其在PNI修复中的靶向干预潜力,为开发新型治疗策略提供更坚实的理论基础。
Following peripheral nerve injury(PNI),ferroptosis participates in neuronal damage and dysfunction via iron-dependent lipid peroxidation.Autophagy,as an intracellular degradation process,can intervene in ferroptosis through multiple pathways by clearing damaged mitochondria and regulating iron homeostasis and the antioxidant system,thereby promoting nerve repair.Especially,mitophagy and ferritinophagy have been confirmed to regulate the occurrence of ferroptosis,making them potential targets for PNIintervention.The current research on the interplay mechanism between autophagy and ferroptosis is still in its initial stage.Future studies can further focus on the role of key autophagy factors in iron homeo stasis regulation and explore their potential for targeted intervention in PNI repair,thereby providing a more solid theoretical basis for developing novel therapeutic strategies.
作者
袁野
王培
YUAN Ye;WANG Pei(Chengde Medical University,Chengde 067500,China;Department of Hand and Foot Surgery,Afiliated Hospital of Chengde Medical University,Chengde 067500,China)
出处
《医学综述》
2025年第21期2573-2578,共6页
Medical Recapitulate
基金
河北省科技计划项目(142777105D)
河北省神经损伤与修复重点实验室(SZX2020020)。
关键词
周围神经损伤
神经再生
自噬
铁死亡
线粒体
氧化应激
Peripheral nerve injury
Nerve regeneration
Autophagy
Ferroptosis
Mitochondria
Oxidative stress
