The Role of Ferroptosis in Blood–Brain Barrier Injury

Zhao, Yao; Liu, Ying; Xu, Yunfei; Li, Kexin; Zhou, Lin; Qiao, Haoduo; Xu, Qing; Zhao, Jie

doi:10.1007/s10571-022-01197-5

Cited by 25 publications

(20 citation statements)

References 123 publications

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“…Several neurological disorders can happen due to BBB dysfunction. Ferroptosis can play a key role in BBB dysfunction [15].…”

Section: Ferroptotic Influence On the Manifestation Of Neurological C...mentioning

confidence: 99%

The “Irony” of Ferroptosis: A Review on Neurological Challenges

Munshi¹,

Bhattacharya²

2023

Biochemistry

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Ferroptosis in recent days has gained high impact due to its implication in inducing several neurological challenges. Impairment of iron homeostasis (mainly surplus iron deposition) is the key reason for the induction of the ferroptotic cell death. This type of programmed cell death in the neurons can trigger neuropathological abnormalities. Ferroptosis has been given clinical importance, where biomedical researchers are working on the pathological detection of ferroptosis and finding clinical ways to arrest it. In this review, we have elucidated the impact of ferroptotic cell death on the pathophysiology of several neurological challenges.

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“…Several neurological disorders can happen due to BBB dysfunction. Ferroptosis can play a key role in BBB dysfunction [15].…”

Section: Ferroptotic Influence On the Manifestation Of Neurological C...mentioning

confidence: 99%

The “Irony” of Ferroptosis: A Review on Neurological Challenges

Munshi¹,

Bhattacharya²

2023

Biochemistry

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“…Iron is an important cofactor in multiple neuronal activities. Under normal physiological conditions, iron levels in the brain are tightly regulated by strict restriction of iron transport across the BBB and the feedback loops of iron levels in the CNS [ 37 ]. A recent study demonstrated in an established BBB injury model of organophosphate paraoxon on a stem-cell-derived in vitro human BBB system that organophosphate-induced BBB breakdown and oxidative stress could be rescued by the iron chelator desferal (DFO).…”

Section: Ferroptosis and The Brainmentioning

confidence: 99%

Iron Brain Menace: The Involvement of Ferroptosis in Parkinson Disease

Lin

Chen

Lin

et al. 2022

Cells

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Parkinson disease (PD) is the second-most common neurodegenerative disease. The characteristic pathology of progressive dopaminergic neuronal loss in people with PD is associated with iron accumulation and is suggested to be driven in part by the novel cell death pathway, ferroptosis. A unique modality of cell death, ferroptosis is mediated by iron-dependent phospholipid peroxidation. The mechanisms of ferroptosis inhibitors enhance antioxidative capacity to counter the oxidative stress from lipid peroxidation, such as through the system xc−/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis and the coenzyme Q10 (CoQ10)/FSP1 pathway. Another means to reduce ferroptosis is with iron chelators. To date, there is no disease-modifying therapy to cure or slow PD progression, and a recent topic of research seeks to intervene with the development of PD via regulation of ferroptosis. In this review, we provide a discussion of different cell death pathways, the molecular mechanisms of ferroptosis, the role of ferroptosis in blood–brain barrier damage, updates on PD studies in ferroptosis, and the latest progress of pharmacological agents targeting ferroptosis for the intervention of PD in clinical trials.

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“…The decomposition of glutamine can produce α-ketoglutarate, which participates in the tricarboxylic acid cycle (TCA) cycle occurring in the mitochondrial matrix and mimic the deathinducing activity of L-Gln, thereby regulating the ferroptosis (Gao et al, 2015). Suppression of TCA cycle or electron transfer chain (ETC) can effectively reduce the production of lipid peroxides (Zhao et al, 2022), thereby reducing the occurrence of ferroptosis, indicating that ferroptosis is related to abnormal ROS production. At the same time, glutamine decomposition can generate intermediates of the TCA cycle which induces mitochondrial membrane hyperpolarization, and it may reflect the increase of ETC activity and ROS generation (Tang E. et al, 2021).…”

Section: Ferroptosis In Mitochondriamentioning

confidence: 99%

The Organelle-Specific Regulations and Epigenetic Regulators in Ferroptosis

Zhang

Guo

et al. 2022

Front. Pharmacol.

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Ferroptosis is fairly different from other types of cell-death in biochemical processes, morphological changes and genetics as a special programmed cell-death. Here we summarize the current literatures on ferroptosis, including the cascade reaction of key material metabolism in the process, dysfunction of organelles, the relationship between different organelles and the way positive and negative key regulatory factors to affect ferroptosis in the epigenetic level. Based on material metabolism or epigenetic regulation, it is obvious that the regulatory network of ferroptosis is interrelated and complex.

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The Role of Ferroptosis in Blood–Brain Barrier Injury

Cited by 25 publications

References 123 publications

The “Irony” of Ferroptosis: A Review on Neurological Challenges

The “Irony” of Ferroptosis: A Review on Neurological Challenges

Iron Brain Menace: The Involvement of Ferroptosis in Parkinson Disease

The Organelle-Specific Regulations and Epigenetic Regulators in Ferroptosis

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