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作 者:Daolin Tang Xin Chen Guido Kroemer
机构地区:[1]Department of Surgery,UT Southwestern Medical Center,Dallas,TX,USA [2]Guangzhou Municipal and Guangdong Provincial Key Laboratory of Protein Modification and Degradation,School of Basic Medical Sciences,Affiliated Cancer Hospital&Institute of Guangzhou Medical University,Guangzhou,Guangdong,China [3]Centre de Recherche des Cordeliers,Equipe labellisée par la Ligue contre le cancer,Universitéde Paris,Sorbonne Université,INSERM U1138,Institut Universitaire de France,Paris,France [4]Metabolomics and Cell Biology Platforms,Gustave Roussy Cancer Campus,Villejuif,France [5]Pôle de Biologie,Hôpital Européen Georges Pompidou,AP-HP,Paris,France
出 处:《Cell Research》2022年第5期417-418,共2页细胞研究(英文版)
摘 要:Various heavy metals can induce regulated cell death through different subroutines.A recent study published in Science found that intracellular copper accumulation triggers the aggregation of mitochondrial lipoylated proteins and the destabilization of Fe–S cluster proteins,leading to a unique type of cell death termed cuproptosis.Beyond classical apoptosis,several forms of regulated cell death(RCD)have been identified.These RCD subroutines differ in the initiating stimuli,intermediate activation events,and end effectors.1 Heavy metal ions are essential micronutrients,but either insufficient or excessive abundance of metals can trigger cell death.For example,ferroptosis has been defined as an iron-dependent form of oxidative cell death caused by unrestricted lipid peroxidation.2 Surprisingly,a recent study by Tsvetkov and colleagues showed that intracellular copper(Cu)induces a novel form of RCD that is different from oxidative stress-related cell death(e.g.,apoptosis,ferroptosis,and necroptosis)and has been termed“cuproptosis”.3 In contrast,mitochondrial stress,especially the aggregation of lipoylated mitochondrial enzymes and the loss of Fe–S cluster proteins,ignites cuproptosis(Fig.1).
关 键 词:DEATH ROUTINE PEROXIDATION
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