Elucidating the progress and impact of ferroptosis in hemorrhagic stroke

Pan, Feixia; Xu, Wei; Ding, Jieying; Wang, Chencen

doi:10.3389/fncel.2022.1067570

Cited by 16 publications

(8 citation statements)

References 139 publications

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“…Of note, ferroptosis is a ROS-dependent form of cell death characterized by iron accumulation and lipid peroxidation [ 5 , 22 ] The lipid peroxidation is a free radical-driven reaction that primarily affects polyunsaturated fatty acids in cell membranes, the product of which gradually increases during ferroptosis, from the initial lipid hydroperoxides (LOOHs) to the later production of malondialdehyde (MDA) and 4-hydroxynenoals (4-HNE) [ 5 , 6 ]. Disruption of the antioxidant systems is contributed to overproduction and accumulation of lipid peroxidation products.…”

Section: Discussionmentioning

confidence: 99%

“…Another efficient endogenous antioxidant system is the ferroptosis suppressor protein 1 (FSP1)/coenzyme Q10 (CoQ10) pathway [ 12 ]. FSP1 uses the reducing equivalents of NADP [NAD(P)H] to reduce CoQ10 to ubiquinol, which acts as a lipophilic radical-trapping antioxidant to remove lipid peroxides from phospholipid bilayers [ 12 , 22 ]. In our study, we demonstrated that GSH deletion and MDA accumulation in SAH was improved by Fer-1treatment, the mechanism under which may be associated with both GSH/GPX4 and FSP1/CoQ10 antioxidant system.…”

Section: Discussionmentioning

confidence: 99%

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Ferrostatin-1 attenuates brain injury in animal model of subarachnoid hemorrhage via phospholipase A2 activity of PRDX6

et al. 2023

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Subarachnoid hemorrhage (SAH) is an acute catastrophic neurological disorder with high morbidity and mortality. Ferroptosis is one of the pathophysiological processes during secondary brain injury of SAH, which could be inhibited by ferrostatin-1 (Fer-1) effectively. Peroxiredoxin6 (PRDX6) is an antioxidant protein and is currently proven to be associated with lipid peroxidation in ferroptosis except in GSH/GPX4 and FSP1/CoQ10 antioxidant systems. However, the alteration and function of PRDX6 in SAH are still unknown. In addition, whether PRDX6 is involved in the neuroprotection of Fer-1 in SAH is yet to be investigated. Endovascular perforation was employed to induce the SAH model. Fer-1 and in vivo siRNA aiming to knockdown PRDX6 were administrated intracerebroventricularly to investigate relevant regulation and mechanism. We confirmed the inhibition of ferroptosis and neuroprotection from brain injury by Fer-1 in SAH. The induction of SAH reduced the expression of PRDX6, which could be alleviated by Fer-1. Accordingly, dysregulated lipid peroxidation indicated by GSH and MDA was improved by Fer-1, which was counteracted by si-PRDX6. Similarly, the neuroprotection of Fer-1 in SAH was diminished by the knockdown of PRDX6 and the administration of a calcium-independent phospholipase A2 (iPLA2) inhibitor. PRDX6 is involved in ferroptosis induced by SAH and is associated with Fer-1 neuroprotection from brain injury via its iPLA2 activity.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Ferrostatin-1 attenuates brain injury in animal model of subarachnoid hemorrhage via phospholipase A2 activity of PRDX6

et al. 2023

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“…Morphologically, ferroptosis is characterized by mitochondrial contraction and increased mitochondrial membrane density. 56,57 Unlike other cell death types, there is no cell swelling or membrane rupture, and no changes in the nucleus or chromatin contraction are observed. Biochemically, ferroptosis involves the aggregation of reactive oxygen species and iron ions, activation of the mitogen-activated protein kinase (MAPK) system, reduced cystine uptake, depletion of glutathione, and inhibition of system Xc − , among others.…”

Section: Ferroptosis and Its Process Overview Of Ferroptosismentioning

confidence: 99%

Advances in Ferroptosis-Inducing Agents by Targeted Delivery System in Cancer Therapy

Xiang,

Zhou,

Yang

et al. 2024

IJN

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Currently, cancer remains one of the most significant threats to human health. Treatment of most cancers remains challenging, despite the implementation of diverse therapies in clinical practice. In recent years, research on the mechanism of ferroptosis has presented novel perspectives for cancer treatment. Ferroptosis is a regulated cell death process caused by lipid peroxidation of membrane unsaturated fatty acids catalyzed by iron ions. The rapid development of bio-nanotechnology has generated considerable interest in exploiting iron-induced cell death as a new therapeutic target against cancer. This article provides a comprehensive overview of recent advancements at the intersection of iron-induced cell death and bionanotechnology. In this respect, the mechanism of iron-induced cell death and its relation to cancer are summarized. Furthermore, the feasibility of a nano-drug delivery system based on iron-induced cell death for cancer treatment is introduced and analyzed. Secondly, strategies for inducing iron-induced cell death using nanodrug delivery technology are discussed, including promoting Fenton reactions, inhibiting glutathione peroxidase 4, reducing low glutathione levels, and inhibiting system Xc − . Additionally, the article explores the potential of combined treatment strategies involving iron-induced cell death and bionanotechnology. Finally, the application prospects and challenges of iron-induced nanoagents for cancer treatment are discussed.

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“…Biochemical and transcriptomic analyses of mediators of iron metabolism, antioxidant defenses, oxidative stress, and lipid peroxidation in experimental disease models, autopsy material, and induced pluripotent stem cell (iPSCs) derived from patients indicate that ferroptosis is a major mechanism of cell death in a wide range of neurologic disorders. These include Alzheimer disease (AD), 64,72,76-82 Parkinson disease (PD), 55,83-87 amyotrophic lateral sclerosis (ALS), 88-92 Huntington disease, 93-95 Friedreich ataxia, 96-98 multiple sclerosis, 99-101 ischemic stroke, 47,102-105 intracerebral hemorrhage, 106,107 traumatic brain injury, 108 spinal cord injury, 109,110 epilepsy, 111-113 and glioma, 114 among others. This topic has been extensively reviewed, 16-21,115,116 and only few concepts will be emphasized in this study.…”

Section: Role Of Ferroptosis In Neurologic Diseasementioning

confidence: 99%

What Is the Role of Ferroptosis in Neurodegeneration?

Benarroch

2023

Neurology

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Ferroptosis is a unique form of programmed cell death pathway that is mechanistically different from necrosis, apoptosis, or autophagy.1 Ferroptosis is induced by reactive oxygen species (ROS) originating from multiple sources, especially accumulation of free intracellular divalent iron (Fe2+), leading to peroxidation of polyunsaturated fatty acids (PUFAs) and resulting in membrane damage (Figure). One major trigger of ferroptosis is decreased availability of intracellular antioxidant enzymes, particularly glutathione peroxidases (GPXs).1-7 Because of its high lipid concentration and oxygen consumption rate, the nervous tissue is extremely vulnerable to oxidative damage and ferroptosis. With aging, iron accumulates in the brain, which predisposes to and exacerbates these processes.8 Iron promotes ferroptosis both directly and as a cofactor required for the activity of enzymes mediating redox reactions and lipid peroxidation.9,10 Epigenetic regulation can determine cell sensitivity to ferroptosis by affecting intracellular iron levels, oxidative stress, and lipid metabolism.11 Ferroptosis affects all cell types in the nervous system, including neurons, glial cells, and pericytes.12 Microglia are the primary iron-accumulating cells in disease.13,14 Recent evidence indicates that iron-laden microglia have a critical role in ferroptosis associated with neurodegeneration.15 Studies in vitro, in experimental disease models, and in human brain tissue indicate that iron accumulation, oxidative stress, and lipid peroxidation are major disease mechanisms in a wide range of neurologic disorders. These studies also suggest that the different components of the ferroptosis pathway are potential targets for therapeutic intervention. The mechanisms of ferroptosis and its role in neurologic disorders have been the subject of several recent comprehensive reviews.7,8,16-21 Some of these concepts pertinent to neurodegeneration will be emphasized in this study.

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Elucidating the progress and impact of ferroptosis in hemorrhagic stroke

Cited by 16 publications

References 139 publications

Ferrostatin-1 attenuates brain injury in animal model of subarachnoid hemorrhage via phospholipase A2 activity of PRDX6

Ferrostatin-1 attenuates brain injury in animal model of subarachnoid hemorrhage via phospholipase A2 activity of PRDX6

Advances in Ferroptosis-Inducing Agents by Targeted Delivery System in Cancer Therapy

What Is the Role of Ferroptosis in Neurodegeneration?

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