摘要
帕金森病(Parkinson disease,PD)是一种以肌强直、静止性震颤和运动迟缓为主要表现的神经退行性疾病。研究表明,铁死亡作为一种由铁代谢紊乱和氧化应激引发的新型细胞死亡方式,在PD发病中起关键作用。运动作为一种安全的非药物干预手段,可通过激活核因子E2相关因子2(nuclear factor E2-related factor 2,Nrf2)/脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)信号通路,增强抗氧化能力、调控铁代谢,进而抑制铁死亡,改善神经元功能。本文综述铁死亡在PD中的作用及运动调控的机制,为PD防治提供参考资料。
Parkinson disease(PD)is a prevalent neurodegenerative disorder,clinically characterized by symptoms such as muscle rigidity,resting tremor,and bradykinesia.Recent studies have indicated that ferroptosis,a newly identified form of cell death,may play a critical role in the pathogenesis of PD.This process is initiated by disorders in iron metabolism and oxidative stress,which ultimately lead to neuronal dysfunction.Exercise,recognized as a safe and effective non-pharmacological intervention,has the potential to activate the nuclear factor E2-related factor 2(Nrf2)/brainderived neurotrophic factor(BDNF)signaling pathway,enhance antioxidant capacity,and regulate iron metabolism.These effects collectively inhibit the onset of ferroptosis and improve neuronal function.This article systematically reviews the mechanisms of ferroptosis in PD and discusses in detail how exercise may regulate ferroptosis through the Nrf2/BDNF pathway.The aim is to provide a new theoretical framework and clinical intervention strategies for the prevention and treatment of PD.
作者
卢冬磊
曹立全
谭思洁
LU Donglei;CAO Liquan;TAN Sijie(Tianjin Key Laboratory of Sports and Health Integration and Health Promotion,Tianjin 301617,Ch)
出处
《中国病理生理杂志》
北大核心
2025年第12期2465-2472,共8页
Chinese Journal of Pathophysiology
基金
科技部国家重点研发计划(No.2020YFC2006704)。
