中国药理学与毒理学杂志2025，Vol.39Issue(12)：923-932,10.DOI:10.3867/j.issn.1000-3002.2025.08699
线粒体自噬与铁死亡的分子机制及其在阿尔茨海默病中的相互作用研究进展
Research progress in molecular mechanisms of mitophagy and ferroptosis and their interactions in Alzheimer disease
摘要
Abstract
Alzheimer disease(AD)is a neurodegenerative disorder characterized by the deposition of amyloid β-protein(Aβ)and the formation of neurofibrillary tangles of tau protein.Mitophagy and ferroptosis have been identified as key drivers of this disease.In AD,impaired mitophagy disrupts intra-cellular redox and iron homeostasis,potentially increasing the susceptibility of neurons to ferroptosis.Conversely,ferroptosis-related events can exacerbate mitochondrial dysfunction,and the resulting vicious cycle is considered an important mechanism for accelerating the progression of the disease.In other words,mitophagy dysfunction may be a significant inducer of ferroptosis,and targeting their inter-action network may provide new strategies for AD treatment.This paper reviews the molecular mecha-nisms of mitophagy and ferroptosis in general and their complex interactions in AD in particular.Based on this interaction network,this paper summarizes some potential therapeutic strategies,such as urolithin A and ferroptosis inhibitors in the hope of providing a reference for the development of novel intervention programs for AD.关键词
阿尔茨海默病/线粒体自噬/铁死亡/氧化应激/自噬/铁沉积Key words
Alzheimer disease/mitochondrial autophagy/ferroptosis/oxidative stress/autophagy/iron deposition分类
医药卫生引用本文复制引用
刘安南,李建辉,高伟,邢丽萍,宋婧,姚明远,李虹霖..线粒体自噬与铁死亡的分子机制及其在阿尔茨海默病中的相互作用研究进展[J].中国药理学与毒理学杂志,2025,39(12):923-932,10.基金项目
国家自然科学基金(82105035) （82105035）
黑龙江省自然科学基金(LH2023H064) National Natural Science Foundation of China(82105035) （LH2023H064）
and Natural Science Foundation of Hei-longjiang Province(LH2023H064) （LH2023H064）
