Ferritinophagy is Involved in Experimental Subarachnoid Hemorrhage-Induced Neuronal Ferroptosis

Liang, Yaxuan; Deng, Yongbing; Zhao, Jun; Liu, Liu; Wang, Jia; Chen, Peng; Zhang, Qingtao; Sun, Chao; Wang, Yanglingxi; Xiang, Yang; He, Zhaohui

doi:10.1007/s11064-021-03477-w

Cited by 25 publications

(16 citation statements)

References 23 publications

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“…[336] A recent study showed that ferritinophagy is involved in the pathogenesis of EBI-SAH through inducing ferroptosis. [337] As a type of autophagy, ferritinophagy mediated by nuclear receptor activator 4 (NCOA4) plays a role in inducing ferroptosis by regulating iron homeostasis and producing ROS in cells. [338][339][340] NCOA4 acts as a selective autophagy receptor and binds to FTH1 of ferritin to mediate the transport of intracellular ferritin to autophagy lysosomes and finally releases free iron, which increases the content of available iron in cells.…”

Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

Wang

et al. 2023

Advanced Science

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Emerging evidence suggests that ferroptosis, a unique regulated cell death modality that is morphologically and mechanistically different from other forms of cell death, plays a vital role in the pathophysiological process of neurodegenerative diseases, and strokes. Accumulating evidence supports ferroptosis as a critical factor of neurodegenerative diseases and strokes, and pharmacological inhibition of ferroptosis as a therapeutic target for these diseases. In this review article, the core mechanisms of ferroptosis are overviewed and the roles of ferroptosis in neurodegenerative diseases and strokes are described. Finally, the emerging findings in treating neurodegenerative diseases and strokes through pharmacological inhibition of ferroptosis are described. This review demonstrates that pharmacological inhibition of ferroptosis by bioactive small‐molecule compounds (ferroptosis inhibitors) could be effective for treatments of these diseases, and highlights a potential promising therapeutic avenue that could be used to prevent neurodegenerative diseases and strokes. This review article will shed light on developing novel therapeutic regimens by pharmacological inhibition of ferroptosis to slow down the progression of these diseases in the future.

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Section: Subarachnoid Hemorrhagementioning

confidence: 99%

Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

Wang

et al. 2023

Advanced Science

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“… 94 Knockdown of coatomer protein complex subunit zeta 1 (COPZ1) can induce ferroptosis in glioblastoma cells by upregulating NCOA4 and promoting ferritinophagy. 34 Ferritinophagy to promote cellular ferroptosis has also been found to be involved in subarachnoid hemorrhage (SAH) in rats 95 . Chaperone-mediated autophagy (CMA) is an autophagic process in which substrate proteins in the cytosol are selectively bound by molecular chaperones and transported into lysosomes for digestion and degradation by lysosomal enzymes.…”

Section: Potential Regulatory Mechanisms Of Ferroptosismentioning

confidence: 99%

Ferroptosis and Its Potential Role in the Nervous System Diseases

Zhou¹,

Lin²,

Rao³

et al. 2022

JIR

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Ferroptosis is a novel regulated cell death characterized by metabolic disorders and iron-dependent oxidative destruction of the lipid bilayer. It is primarily caused by the imbalance of oxidation and anti-oxidation in the body and is precisely regulated by numerous factors and pathways inside and outside the cell. Recent studies have indicated that ferroptosis plays a vital role in the pathophysiological process of multiple systems of the body including the nervous system. Ferroptosis may be closely linked to the occurrence and development of neurodegenerative diseases, strokes, and brain tumors. It may also be involved in the development, maturation, and aging of the nervous system. Therefore, this study aims to investigate ferroptosis's occurrence and regulatory mechanism and summarize its research progress in the pathogenesis and treatment of neurological diseases. This would allow for novel ideas for basic and clinical research of neurological diseases.

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“…Baicalin treatment down-regulated the expression of Beclin1 protein and microtubule-associated protein 1 light chain 3-II (LC3-II) and down-regulated the levels of Fe2+ and MDA in the brain of SAH rats; this suggested that baicalin exerted a brain-protective effect by inhibiting autophagy-dependent ferroptosis in SAH ( 109 ). Liang et al ( 110 ) revealed that ferroptosis induced by SAH was autophagy-dependent. Knockout of the autophagy-related gene ATG5 inhibited autophagy, decreased the levels of intracellular iron and lipid peroxidation, augmented the levels of anti-ferroptosis protein, and significantly improved the prognostic index with SAH.…”

Section: Crosstalk Between Ferroptosis and Other Pathologic Processes...mentioning

confidence: 99%

Ferroptosis—A Novel Mechanism With Multifaceted Actions on Stroke

Fang

Ding

et al. 2022

Front. Neurol.

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As a neurological disease with high morbidity, disability, and mortality, the pathological mechanism underlying stroke involves complex processes such as neuroinflammation, oxidative stress, apoptosis, autophagy, and excitotoxicity; but the related research on these molecular mechanisms has not been effectively applied in clinical practice. As a form of iron-dependent regulated cell death, ferroptosis was first discovered in the pathological process of cancer, but recent studies have shown that ferroptosis is closely related to the onset and development of stroke. Therefore, a deeper understanding of the relationship between ferroptosis and stroke may lead to more effective treatment strategies. Herein, we reviewed the mechanism(s) underlying the onset of ferroptosis in stroke, the potential role of ferroptosis in stroke, and the crosstalk between ferroptosis and other pathological mechanisms. This will further deepen our understanding of ferroptosis and provide new approaches to the treatment of stroke.

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Ferritinophagy is Involved in Experimental Subarachnoid Hemorrhage-Induced Neuronal Ferroptosis

Cited by 25 publications

References 23 publications

Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

Pharmacological Inhibition of Ferroptosis as a Therapeutic Target for Neurodegenerative Diseases and Strokes

Ferroptosis and Its Potential Role in the Nervous System Diseases

Ferroptosis—A Novel Mechanism With Multifaceted Actions on Stroke

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