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The pathological role of ferroptosis in ischemia/reperfusion-related injury

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Zoological Research 2020年第3期41卷 220-230页

作者： Hong-Fa Yan qing-zhang tuo Qiao-Zhi Yin Peng Lei Department of Neurology and State Key Laboratory of Biotherapy West China HospitalSichuan Universityand Collaborative Center for BiotherapyChengduSichuan 610041China Chengdu University of Traditional Chinese Medicine ChengduSichuan 610041China

Ischemia/reperfusion(I/R) is a pathological process that occurs in numerous organs throughout the human body, and it is frequently associated with severe cellular damage and death. Recently it has emerged that ferroptosis, a new form of regulated cell death that is caused by iron-dependent lipid peroxidation, plays a significantly detrimental role in many I/R models. In this review, we aim to revise the pathological process of I/R and then explore the molecular pathogenesis of ferroptosis. Furthermore,we aim to evaluate the role that ferroptosis plays in I/R, providing evidence to support the targeting of ferroptosis in the I/R pathway may present as a therapeutic intervention to alleviate ischemia/reperfusion injury(IRI) associated cell damage and death.

关键词： Ischemia/reperfusion Ferroptosis Reactive oxygen species Lipid peroxidation Iron

Ferroptosis:mechanisms and links with diseases

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Signal Transduction and Targeted Therapy 2021年第3期6卷 648-663页

作者： Hong-fa Yan Ting Zou qing-zhang tuo Shuo Xu Hua Li Abdel Ali Belaidi Peng Lei Department of Neurology and State Key Laboratory of Biotherapy West China HospitalSichuan Universityand Collaborative Center for Biotherapy610041 ChengduChina West China School of Basic Medical Sciences and Forensic Medicine Sichuan University610041 ChengduChina Melbourne Dementia Research Centre and the Florey Institute of Neuroscience and Mental Health The University of MelbourneParkvilleVIC 3052Australia

Ferroptosis is an iron-dependent cell death,which is different from apoptosis,necrosis,autophagy,and other forms of cell *** process of feroptotic cell death is defined by the accumulation of lethal lipid species derived from the peroxidation of lipids,which can be prevented by iron chelators(***,deferoxamine)and small lipophilic antioxidants(e.g,ferrostatin,liproxstatin).This review summarizes current knowledge about the regulatory mechanism of ferroptosis and its association withseveral pathways,including iron,lipid,and cysteine *** have further discussed the contribution of ferroptosis to thepathogenesis of several diseases such as cancer,ischemia/reperfusion,and various neurodegenerative diseases(*** and Parkinson's disease),and evaluated the therapeutic applications of ferroptosis inhibitors in clinics.

关键词： diseases peroxidation death

Iron promotes both ferroptosis and necroptosis in the early stage of reperfusion in ischemic stroke

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Genes & Diseases 2024年第6期11卷 495-509页

作者： Bin Du Zijie Deng Kang Chen zhangzhong Yang Junfen Wei Liuyao Zhou Jie Meng Ying Cheng Xin Tian qing-zhang tuo Peng Lei Department of Neurology and State Key Laboratory of Biotherapy National Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityChengduSichuan 610041China Department of Neurology First Affiliated Hospital of Chongqing Medical UniversityChongqing Key Laboratory of NeurologyChongqing 400016China

Programmed cell death contributes to neurological damage in ischemic stroke,especially during the reperfusion *** cell death pathways have been tested preclinically and clinically,including ferroptosis,necroptosis,and ***,the sequence and complex interplay between cell death pathways during ischemia/reperfusion remains under ***,we unbiasedly investigated cell death pathways during ischemia/reperfusion by utilizing RNA sequencing analysis and immunoblot assays and revealed that ferroptosis and necroptosis occurred early post-reperfusion,followed by *** inhibitor Liproxstatin-1 effectively inhibited necroptosis during reperfusion,while the necroptosis inhibitor Necrostatin-1 suppressed protein expression consistent with ferroptosis ***–protein interaction analysis and iron chelation therapy by deferoxamine mesylate indicate that iron is capable of promoting both ferroptosis and necroptosis in middle cerebral artery occlusion/repression modeled *** of cells with iron led to a disruption in redox balance with activated necroptosis and increased susceptibility to ***,these data uncovered a complex interplay between ferroptosis and necroptosis during ischemic stroke and indicated that multiple programmed cell death pathways may be targeted co-currently.

关键词： Deferoxamine Ferroptosis Iron Ischemic stroke Necroptosis

Ferroptosis promotes T-cell activation-induced neurodegeneration in multiple sclerosis

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Cellular & Molecular Immunology 2022年第8期19卷 913-943页

作者： Jinyuan Luoqian Wenyong Yang Xulong Ding qing-zhang tuo Zheng Xiang Zhaoyue Zheng Yu-jie Guo Li Li Pengbo Guan Scott Ayton Biao Dong Huiyuan zhang Hongbo Hu Peng Lei Department of Neurology and Center for Immunology and Hematology State Key Laboratory of BiotherapyNational Clinical Research Center for GeriatricsWest China HospitalSichuan UniversityCollaborative Innovation Center for BiotherapyChengduSichuanChina Melbourne Dementia Research Centre Florey Institute of Neuroscience and Mental HealthThe University of MelbourneParkvilleVICAustralia

While many drugs are effective at reducing the relapse frequency of multiple sclerosis (MS), there is an unmet need for treatments that slow neurodegeneration resulting from secondary disease progression. The mechanism of neurodegeneration in MS has not yet been established. Here, we discovered a potential pathogenetic role of ferroptosis, an iron-dependent regulated cell death mechanism, in MS. We found that critical ferroptosis proteins (acyl-CoA synthetase long-chain family member 4, ACSL4) were altered in an existing genomic database of MS patients, and biochemical features of ferroptosis, including lipid reactive oxygen species (ROS) accumulation and mitochondrial shrinkage, were observed in the experimental autoimmune encephalitis (EAE) mouse model. Targeting ferroptosis with ferroptosis inhibitors or reducing ACSL4 expression improved the behavioral phenotypes of EAE mice, reduced neuroinflammation, and prevented neuronal death. We found that ferroptosis was an early event in EAE, which may promote T-cell activation through T-cell receptor (TCR) signaling in vitro and in vivo. These data indicate that ferroptosis may be a potential target for treating MS.

关键词： Ferroptosis Multiple sclerosis EAE Neurodegeneration ACSL4

Iron is a critical factor in focal cerebral ischemia-reperfusion injury

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Iron is a critical factor in focal cerebral ischemia-reperfu...

Neuroprotection of ceruloplasmin on experimental stroke model

中国神经科学学会第十二届全国学术会议

作者： qing-zhang tuo Peng Lei Department of Neurology and State Key Laboratory of Biotherapy West China HospitalSichuan University

Background: Clinical studies have shown that disturbance of iron homeostasis in ischemic stroke influenced recovery and functional outcome following blood reperfusion of obstructed cerebral vessels, but the mechanism of iron-mediated toxicity in ischemic strokes has not been fully elucidated. Methods: A middle cerebral artery occlusion（MCAO） mouse model was established by introducing an embolus into the middle cerebral artery, with or without intravenous injection of a potent iron chelator SIH and iron transport protein APPec after MCAO/*** neurological deficit was evaluated by a five-point scale. After 24 hours of reperfusion, mice were sacrificed and brains were separated. TTC staining and Nissl staining were performed respectively to detect the area of brain infarction and hippocampal CA1 neuronal survival rate. Mouse tissue metal content was measured by inductively coupled plasma mass spectrometry（ICP-MS） in the lesioned hemisphere 6 hours after reperfusion in mouse MCAO model. Results: Iron level was significantly increased in the lesioned hemisphere 6 hours after reperfusion in mouse MCAO model of ischemic stroke. A potent iron chelator, SIH significantly prevented MCAO-induced behavioral deficits and brain infarct volumes at 24 h post-reperfusion. APPec showed protective effect on ischemia/reperfusion injury, and could prevent iron accumulation in the lesioned hemisphere after MCAO without altering the iron content in the unlesioned hemisphere. Conclusions: This study indicates that iron overload is the main cause of neuronal injury after focal cerebral ischemia/reperfusion, and the accumulation of iron could due to insufficient iron export.

关键词： iron iron overload MCAO ischemia/reperfusion stroke

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Neuroprotection of ceruloplasmin on experimental stroke mode...

Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion

中国神经科学学会第十二届全国学术会议

作者： Xu-long Ding qing-zhang tuo Peng Lei State Key Laboratory of Biotherapy West China Hospital Sichuan University

Background: Cerebrovascular disease(CVD) is one of the three illnesses which cause most deaths all over the world. In cerebrovascular diseases, ischemic stroke has the highest incidence. The current clinical treatment program for ischemic stroke cannot fundamentally handle high mortality and high morbidity after the onset of ischemic stroke, so it’s urgent that we need a more effective treatment to cure ischemic stroke. Ceruloplasmin(Cp) can oxidize Fe to Fe, and preventing Fe to cause damage therefore may be able to rescue ischemia/reperfusion ***: We established middle cerebral artery occlusion(MCAO) mice model, divided MCAO mice into three groups randomly, and injected with saline, ceruloplasmin and Apo-ceruloplasmin(Apo-Cp) respectively. The neurological function of MCAO model mice was evaluated by Bederson score method. The movement coordination ability was evaluated by rotarod test. The hippocampal Cp was detected by western blot and the activity was detected by Fe acquisition and Fe loss assays. The area of cerebral infarction was observed by TTC staining at 24 hours after ischemia-reperfusion. Results: The neurological function of MCAO mice treated with Cp was significantly improved compared with the mice with saline. Cp expression in ischemic site of MCAO mice was significantly increased compared with non-ischemic site, but the activity was unchanged. The TTC staining showed that the cerebral infarction area of MCAO model mice treated with Cp was significantly lower than the saline group. MCAO mice treated with Apo-Cp showed no improvement. Conclusions: Ceruloplasmin can rescue the ischemia/reperfusion injury, which should be explored further as drug candidate.

关键词： Ischemic Stroke ceruloplasmin MCAO Neuroprotection

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Signal Transduction and Targeted Therapy 2022年第3期7卷 881-895页

作者： qing-zhang tuo Yu Liu Zheng Xiang Hong-Fa Yan Ting Zou Yang Shu Xu-long Ding Jin-jun Zou Shuo Xu Fei Tang Yan-qiu Gong Xiao-lan Li Yu-jie Guo Zhao-yue Zheng Ai-ping Deng zhang-zhong Yang Wen-jing Li Shu-ting zhang Scott Ayton Ashley I.Bush Heng Xu Lunzhi Dai Biao Dong Peng Lei Department of Geriatrics and State Key Laboratory of Biotherapy National Clinical Research Center for GeriatricsWest China HospitalSichuan University610041 ChengduSichuanChina Department of Neurology and State Key Laboratory of Biotherapy West China HospitalSichuan University610041 ChengduSichuanChina West China School of Basic Medical Sciences and Forensic Medicine Sichuan University610041 ChengduSichuanChina Department of Laboratory Medicine Precision Medicine CenterState Key Laboratory of BiotherapyWest China HospitalSichuan University610041 ChengduSichuanChina Melbourne Dementia Research Centre Florey Institute of Neuroscience and Mental HealthThe University of MelbourneParkvilleVIC 3010Australia

Ischemic stroke represents a significant danger to human beings,especially the *** are only available to remove the clot,and the mechanism of neuronal death during ischemic stroke is still in *** is increasingly appre... 详细信息

关键词： organs death cerebral ischemia

Effect of pyrite content on chalcopyrite flotation under different regrinding conditions

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International Journal of Minerals,Metallurgy and Materials 2025年第1期32卷 49-57页

作者： Zejun Wang qing Shi Guofan zhang Yuxuan Zhu Binbin Li School of Minerals Processing and Bioengineering Central South UniversityChangsha 410083China Key Laboratory of Hunan Province for Clean and Efficient Utilization of Strategic Calcium-containing Mineral Resources Central South UniversityChangsha 410083China

This study aimed to investigate the effect of varying pyrite(Py)content on copper(Cu)in the presence of different regrinding conditions,which were altered using different types of grinding media:iron,ceramic balls,and their mixture,followed by flotation in the cleaner *** flotation performance of rough Cu concentrate can be improved by changing the regrinding conditions based on the Py *** electron microscopy,X-ray spectrometry,ethylenediaminetetraacetic acid disodium salt extraction,and X-ray photoelectron spectroscopy studies illustrated that when the Py content was high,the use of iron media in regrinding promoted the generation of hydrophilic Fe OOH on the surface of Py and improved the Cu *** ceramic medium with a low Py content prevented excessive Fe OOH from covering the surface of chalcopyrite(Cpy).Electrochemical studies further showed that the galvanic corrosion current of Cpy-Py increased with the addition of Py and became stronger with the participation of iron media.

关键词： chalcopyrite regrinding media pyrite galvanic corrosion flotation

Characteristic changes in astrocyte properties during astrocyte-to-neuron conversion induced by NeuroD1/Ascl1/Dlx2

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Neural Regeneration Research 2025年第6期20卷 1801-1815页

作者： qing He Zhen Wang Yuchen Wang Mengjie Zhu Zhile Liang Kanghong zhang Yuge Xu Gong Chen GHM Institute of CNS Regeneration Jinan UniversityGuangzhouGuangdong ProvinceChina

Direct in vivo conversion of astrocytes into functional new neurons induced by neural transcription factors has been recognized as a potential new therapeutic intervention for neural injury and degenerative disorders. However, a few recent studies have claimed that neural transcription factors cannot convert astrocytes into neurons, attributing the converted neurons to pre-existing neurons mis-expressing transgenes. In this study, we overexpressed three distinct neural transcription factors––NeuroD1, Ascl1, and Dlx2––in reactive astrocytes in mouse cortices subjected to stab injury, resulting in a series of significant changes in astrocyte properties. Initially, the three neural transcription factors were exclusively expressed in the nuclei of astrocytes. Over time, however, these astrocytes gradually adopted neuronal morphology, and the neural transcription factors was gradually observed in the nuclei of neuron-like cells instead of astrocytes. Furthermore,we noted that transcription factor-infected astrocytes showed a progressive decrease in the expression of astrocytic markers AQP4(astrocyte endfeet signal), CX43(gap junction signal), and S100β. Importantly, none of these changes could be attributed to transgene leakage into preexisting neurons. Therefore, our findings suggest that neural transcription factors such as NeuroD1, Ascl1, and Dlx2 can effectively convert reactive astrocytes into neurons in the adult mammalian brain.

关键词： aquaporin-4 Ascl1 astrocyte cortex Dlx2 gap junction glia-to-neuron conversion neural regeneration NeuroD1 reprogramming