The mechanism of cuproptosis in Parkinson’s disease

IF 12.5 1区 医学 Q1 CELL BIOLOGY Ageing Research Reviews Pub Date : 2024-02-02 DOI:10.1016/j.arr.2024.102214
Min Huang , Yong Zhang , Xuehong Liu
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Abstract

Parkinson’s disease (PD) is a neurodegenerative disease with an increased morbidity. The pathogenesis PD has not been fully elucidated, and whatever mechanism is involved, it ultimately leads to dopamine (DA) neuronal apoptosis. Cuproptosis is a novel form of cell death. Its morphology, biochemical properties, and mechanism of action differ from known forms of cell death, such as apoptosis, autophagy, necrosis and pyroptosis. Copper binds to the lipoylated components of the tricarboxylic acid cycle, causing proteotoxic stress that ultimately leads to cellular cuproptosis. PD has biochemical features such as mitochondrial dysfunction and decreased levels of copper and glutathione in brain regions. This is closely related to the cuproptosis mechanism. However, the specific link between the pathogenesis of PD and cuproptosis is unclear. Herein, we summarizes cuproptosis as the cause of DA neuronal death in PD, and the relationship between cuproptosis and the PD pathogenesis. This article provides a research basis for targeted cuproptosis for PD.

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帕金森病的杯突症机制
帕金森病(PD)是一种发病率较高的神经退行性疾病。帕金森病的发病机制尚未完全阐明,无论涉及何种机制,最终都会导致多巴胺(DA)神经元凋亡。杯状细胞凋亡是一种新型的细胞死亡形式。它的形态、生化特性和作用机制不同于已知的细胞死亡形式,如细胞凋亡、自噬、坏死和热凋亡。铜与三羧酸循环中的脂酰化成分结合,造成蛋白毒性应激,最终导致细胞杯突变。帕金森病具有生化特征,如线粒体功能障碍以及脑区铜和谷胱甘肽水平下降。这与杯突症机制密切相关。然而,帕金森病的发病机制与杯突症之间的具体联系尚不清楚。在此,我们总结了杯突症是导致帕金森病中DA神经元死亡的原因,以及杯突症与帕金森病发病机制的关系。本文为针对帕金森病的杯突症提供了研究基础。
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来源期刊
Ageing Research Reviews
Ageing Research Reviews 医学-老年医学
CiteScore
19.80
自引率
2.30%
发文量
216
审稿时长
55 days
期刊介绍: With the rise in average human life expectancy, the impact of ageing and age-related diseases on our society has become increasingly significant. Ageing research is now a focal point for numerous laboratories, encompassing leaders in genetics, molecular and cellular biology, biochemistry, and behavior. Ageing Research Reviews (ARR) serves as a cornerstone in this field, addressing emerging trends. ARR aims to fill a substantial gap by providing critical reviews and viewpoints on evolving discoveries concerning the mechanisms of ageing and age-related diseases. The rapid progress in understanding the mechanisms controlling cellular proliferation, differentiation, and survival is unveiling new insights into the regulation of ageing. From telomerase to stem cells, and from energy to oxyradical metabolism, we are witnessing an exciting era in the multidisciplinary field of ageing research. The journal explores the cellular and molecular foundations of interventions that extend lifespan, such as caloric restriction. It identifies the underpinnings of manipulations that extend lifespan, shedding light on novel approaches for preventing age-related diseases. ARR publishes articles on focused topics selected from the expansive field of ageing research, with a particular emphasis on the cellular and molecular mechanisms of the aging process. This includes age-related diseases like cancer, cardiovascular disease, diabetes, and neurodegenerative disorders. The journal also covers applications of basic ageing research to lifespan extension and disease prevention, offering a comprehensive platform for advancing our understanding of this critical field.
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