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| 1 | Thrombin induces ACSL4-dependent ferroptosis during cerebral ischemia/reperfusion显示文摘Ischemic stroke represents a significant danger to human beings,especially the elderly.Interventions are only available to remove the clot,and the mechanism of neuronal death during ischemic stroke is still in debate.Ferroptosis is increasingly appreciated as a mechanism of cell death after ischemia in various organs. | 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 | 2022 | Signal Transduction and Targeted Therapy2022，7，3： | 2 |
| 2 | Ferroptosis promotes T-cell activation-induced neurodegeneration in multiple sclerosis显示文摘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. | 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 | 2022 | Cellular & Molecular Immunology2022，19，8： | 2 |
| 3 | Increased ndfipl in the substantia nigra of parkinsonian brains is associated with elevated iron levels 显示文摘 | Jason Howitt Amanda M Gysbers Scott Ayton | 2014 | Plos One2014，9，87： | 1 |
| 4 | 修剪神经纤维缠结显示文摘Tau protein (encoded by the MAPT gene) is an attractive therapeutic target for the treatment of Alzheimer’s disease (AD) and other “tauopathies”, where aggregated tau pathology accumulates in neurons. Since tau deposition is strongly associated with cognitive dysfunction in AD, and tau purportedly mediates the toxicity of β-amyloid, therapies developed to reduce tau or its phosphorylation have been tested preclinically and in several small-scale clinical trials[1]. However, caveats for tau-targeting therapy include the limited understanding of its physiological functions and the complicated interactions between its post-translational modifications, aggregation, and cellular toxicity. | 雷鹏 Scott Ayton | 2023 | Science Bulletin2023，68，21： | 0 |
| 5 | Transferrin protects against Parkinsonian neurotoxicity and is deficient in Parkinson’s substantia nigra显示文摘Iron deposition in Parkinson’s disease(PD)is a potential disease-modifying target.We previously showed that supplementation of the iron-exporter,ceruloplasmin,selectively corrected nigral iron elevation in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)model.Ceruloplasmin delivers iron to transferrin(Tf),the extracellular iron-transporting protein.We show that Tf protein levels are decreased in the nigra of post-mortem PD brains compared with controls(−35%;n=10 each).Because Tf traffics iron away from iron-replete tissues,we hypothesized that Tf supplementation could selectively facilitate iron export from the nigra in PD.In cultured neurons,Tf treatment corrected iron accumulation,and subcutaneous Tf to mice ameliorated iron accumulation and motor deficits in the MPTP model of PD.Although these data support a role for Tf in the disease mechanism for PD,and its potential use for correcting disorders of iron overload,Tf therapy also caused systemic iron depletion,which could limit its application for PD. | Scott Ayton Peng Lei Catriona Mclean Ashley I Bush David I Finkelstein | 2016 | Signal Transduction and Targeted Therapy2016，1，1： | 0 |
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