Background: Neurodegenerative diseases are characterized by a gradual decline in motor and/or cognitive function caused by the selective degeneration and loss of neurons in the central nervous system, but their pathological mechanism is still unclear. Previous research has revealed that many forms of cell death, such as apoptosis and necrosis, occur in neurodegenerative diseases. Research in recent years has noticed that there is a new type of cell death in neurodegenerative diseases: ferroptosis. An increasing body of literature provides evidence for an involvement of ferroptosis in neurodegenerative diseases. Summary: In this article, we review a new form of cell death in neurodegenerative diseases: ferroptosis. Ferroptosis is defined as an iron-dependent form of regulated cell death, which occurs through the lethal accumulation of lipid-based reactive oxygen species when glutathione-dependent lipid peroxide repair systems are compromised. Several salient and established features of neurodegenerative diseases (including lipid peroxidation and iron dyshomeostasis) are consistent with ferroptosis, which means that ferroptosis may be involved in the progression of neurodegenerative diseases. In addition, as the center of energy metabolism in cells, mitochondria are also closely related to the regulation of iron homeostasis in the nervous system. At the same time, neurodegenerative diseases are often accompanied by degeneration of mitochondrial activity. Mitochondrial damage has been found to be involved in lipid peroxidation and iron dyshomeostasis in neurodegenerative diseases. Key Messages: Based on the summary of the related mechanisms of ferroptosis, we conclude that mitochondrial damage may affect neurodegenerative diseases by regulating many aspects of ferroptosis, including cell metabolism, iron dyshomeostasis, and lipid peroxidation.

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神经退行性疾病中的线粒体调节铁死亡

背景：神经退行性疾病的特点是中枢神经系统神经元选择性变性和丢失导致运动和/或认知功能逐渐下降，但其病理机制尚不清楚。先前的研究表明，神经退行性疾病中会发生多种形式的细胞死亡，例如细胞凋亡和坏死。近年来的研究注意到，神经退行性疾病中存在一种新型的细胞死亡：铁死亡。越来越多的文献提供了铁死亡与神经退行性疾病有关的证据。摘要：在本文中，我们回顾了神经退行性疾病中一种新的细胞死亡形式：铁死亡。铁死亡被定义为铁依赖形式的受调节细胞死亡，当依赖于谷胱甘肽的脂质过氧化物修复系统受到损害时，这是通过基于脂质的活性氧的致命积累而发生的。神经退行性疾病（包括脂质过氧化和铁稳态失调）的几个显着和既定特征与铁死亡一致，这意味着铁死亡可能参与神经退行性疾病的进展。此外，线粒体作为细胞内能量代谢的中枢，还与神经系统铁稳态的调节密切相关。同时，神经退行性疾病往往伴随着线粒体活性的退化。已发现线粒体损伤与神经退行性疾病中的脂质过氧化和铁稳态失调有关。关键信息：