Ferroptosis in Parkinson's disease: Molecular mechanisms and therapeutic potential

Ding, Xv-shen; Gao, Li; Han, Zheng; Eleuteri, Simona; Shi, Wei; Shen, Yun; Song, Zi-yao; Su, Mingming; Yang, Qian; Qu, Yan; Simon, David K.; Wang, Xue-lian; Wang, Bao

doi:10.1016/j.arr.2023.102077

Cited by 38 publications

(9 citation statements)

References 242 publications

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“…Ferrostatin-1 and liproxstatin-1 are typical lipophilic antioxidants that scavenge lipid peroxides and inhibit ferroptosis. Studies have demonstrated that both iron chelators and lipophilic antioxidants could prevent the progression of PD [ 107 ]. Furthermore, deferoxamine lowers the amounts of IL-6, a major inflammatory cytokine generated during COVID-19 [ 108 ], suggesting that deferoxamine may be used as a medication to treat COVID-19-induced PD.…”

Section: Discussionmentioning

confidence: 99%

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect?

Jia,

Han

2024

Cell Death Discov.

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A rising number of patient cases point to a probable link between SARS-CoV-2 infection and Parkinson’s disease (PD), yet the mechanisms by which SARS-CoV-2 affects the brain and generates neuropsychiatric symptoms in COVID-19 patients remain unknown. Ferroptosis, a distinct iron-dependent non-apoptotic type of cell death characterized by lipid peroxidation and glutathione depletion, a key factor in neurological disorders. Ferroptosis may have a pathogenic role in COVID-19, according to recent findings, however its potential contributions to COVID-19-related PD have not yet been investigated. This review covers potential paths for SARS-CoV-2 infection of the brain. Among these putative processes, ferroptosis may contribute to the etiology of COVID-19-associated PD, potentially providing therapeutic methods.

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Section: Discussionmentioning

confidence: 99%

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect?

Jia,

Han

2024

Cell Death Discov.

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“…Notably, ferroptosis features like iron accumulation, GSH depletion, lipid peroxidation, and an increase in ROS species have been observed in PD. Accordingly, inhibitors of ferroptosis have the potential therapeutic role to protect the nervous system in PD [ 89 , 90 , 91 ].…”

Section: Ferroptosis As a Biological Program: Features And General Me...mentioning

confidence: 99%

Antioxidant Systems as Modulators of Ferroptosis: Focus on Transcription Factors

Punziano,

Trombetti,

Cesaro

et al. 2024

Antioxidants

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Ferroptosis is a type of programmed cell death that differs from apoptosis, autophagy, and necrosis and is related to several physio-pathological processes, including tumorigenesis, neurodegeneration, senescence, blood diseases, kidney disorders, and ischemia–reperfusion injuries. Ferroptosis is linked to iron accumulation, eliciting dysfunction of antioxidant systems, which favor the production of lipid peroxides, cell membrane damage, and ultimately, cell death. Thus, signaling pathways evoking ferroptosis are strongly associated with those protecting cells against iron excess and/or lipid-derived ROS. Here, we discuss the interaction between the metabolic pathways of ferroptosis and antioxidant systems, with a particular focus on transcription factors implicated in the regulation of ferroptosis, either as triggers of lipid peroxidation or as ferroptosis antioxidant defense pathways.

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“…Research indicates that dopamine in the brain could potentially have a positive regulatory effect on GPX4. Therefore, the depletion of dopamine in the brain of individuals with Parkinson's disease (PD) may lead to ferroptosis due to the loss of GPX4 [28]. Furthermore, in epileptic brains, astrocytes modulate xCT/GSH/GPX4 via chemokines, leading to neuronal ferroptosis, possibly associated with synchronous brain firing processes [29].…”

Section: Ferroptosis In Central Neurological Disordersmentioning

confidence: 99%

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

Xu,

Jia,

et al. 2024

Antioxidants

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Central neurological disorders are significant contributors to morbidity, mortality, and long-term disability globally in modern society. These encompass neurodegenerative diseases, ischemic brain diseases, traumatic brain injury, epilepsy, depression, and more. The involved pathogenesis is notably intricate and diverse. Ferroptosis and neuroinflammation play pivotal roles in elucidating the causes of cognitive impairment stemming from these diseases. Given the concurrent occurrence of ferroptosis and neuroinflammation due to metabolic shifts such as iron and ROS, as well as their critical roles in central nervous disorders, the investigation into the co-regulatory mechanism of ferroptosis and neuroinflammation has emerged as a prominent area of research. This paper delves into the mechanisms of ferroptosis and neuroinflammation in central nervous disorders, along with their interrelationship. It specifically emphasizes the core molecules within the shared pathways governing ferroptosis and neuroinflammation, including SIRT1, Nrf2, NF-κB, Cox-2, iNOS/NO·, and how different immune cells and structures contribute to cognitive dysfunction through these mechanisms. Researchers’ findings suggest that ferroptosis and neuroinflammation mutually promote each other and may represent key factors in the progression of central neurological disorders. A deeper comprehension of the common pathway between cellular ferroptosis and neuroinflammation holds promise for improving symptoms and prognosis related to central neurological disorders.

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Ferroptosis in Parkinson's disease: Molecular mechanisms and therapeutic potential

Cited by 38 publications

References 242 publications

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect?

COVID-19 related neurological manifestations in Parkinson’s disease: has ferroptosis been a suspect?

Antioxidant Systems as Modulators of Ferroptosis: Focus on Transcription Factors

The Interplay between Ferroptosis and Neuroinflammation in Central Neurological Disorders

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