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| 1 | The molecular machinery of regulated cell death显示文摘Cells may die from accidental cell death(ACD)or regulated cell death(RCD).ACD is a biologically uncontrolled process,whereas RCD involves tightly structured signaling cascades and molecularly defined effector mechanisms.A growing number of novel nonapoptotic forms of RCD have been identified and are increasingly being implicated in various human pathologies.Here,we critically review the current state of the art regarding non-apoptotic types of RCD,including necroptosis,pyroptosis,ferroptosis,entotic cell death,netotic cell death,parthanatos,lysosome-dependent cell death,autophagy-dependent cell death,alkaliptosis and oxeiptosis.The in-depth comprehension of each of these lethal subroutines and their intercellular consequences may uncover novel therapeutic targets for the avoidanee of pathogenic cell loss. | Daolin Tang Rui Kang Tom Vanden Berghe Peter Vandenabeele Guido Kroemer | 2019 | Cell Research2019，29，5： | 143 |
| 2 | Ferroptosis:molecular mechanisms and health implications显示文摘Cell death can be executed through different subroutines.Since the description of ferroptosis as an iron-dependent form of nonapoptotic cell death in 2012,there has been mounting interest in the process and function of ferroptosis.Ferroptosis can occur through two major pathways,the extrinsic or transporter-dependent pathway and the intrinsic or enzyme-regulated pathway.Ferroptosis is caused by a redox imbalance between the production of oxidants and antioxidants,which is driven by the abnormal expression and activity of multiple redox-active enzymes that produce or detoxify free radicals and lipid oxidation products.Accordingly,ferroptosis is precisely regulated at multiple levels,including epigenetic,transcriptional,posttranscriptional and posttranslational layers.The transcription factor NFE2L2 plays a central role in upregulating anti-ferroptotic defense,whereas selective autophagy may promote ferroptotic death.Here,we review current knowledge on the integrated molecular machinery of ferroptosis and describe how dysregulated ferroptosis is involved in cancer,neurodegeneration,tissue injury,inflammation,and infection. | Daolin Tang Xin Chen Rui Kang Guido Kroemer | 2021 | Cell Research2021，31，2： | 182 |
| 3 | Mitochondrial metabolism and cancer显示文摘Glycolysis 长在癌症房间为精力生产和 anabolism 的生长被看作了主要新陈代谢的过程。尽管如此的一个看法为仍然在诊所被使用的强大的成像工具的发展是有帮助的,线粒体在 oncogenesis 起一个关键作用,现在是清楚的。除施加中央 bioenergetic 函数以外,线粒体确实为肿瘤同化提供积木,控制氧化还原作用和钙动态平衡,参予 transcriptional 规定,并且管理房间死亡。因此,线粒体为新奇 anticancer 代理人的发展组成有希望的目标。然而,肿瘤产生,进行,并且回答功能依靠未经触动的 mitochondrial 新陈代谢到在有主人免疫系统,和许多免疫学的亲密串音的上下文的治疗。这里,我们考察房间内在的癌症和线粒体影响都 oncogenesis 通过走的房间外来的机制,与指向为癌症治疗的 mitochondrial 新陈代谢的治疗学的潜力的一个焦点。 | Paolo Ettore Porporato Nicoletta Filigheddu José Manuel Bravo-San Pedro, Guido Kroemer, Lorenzo Galluzzi José Manuel Bravo-San Pedro, Guido Kroemer José Manuel Bravo-San Pedro, Guido Kroemer José Manuel Bravo-San Pedro, Guido Kroemer José Manuel Bravo-San Pedro, Guido Kroemer Guido Kroemer Guido Kroemer Lorenzo Galluzzi Lorenzo Galluzzi | 2018 | Cell Research2018，28，3： | 33 |
| 4 | Cuproptosis:a copper-triggered modality of mitochondrial cell death显示文摘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). | Daolin Tang Xin Chen Guido Kroemer | 2022 | Cell Research2022，32，5： | 19 |
| 5 | Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25显示文摘堵住抗体 ipilimumab 的细胞毒素的 T 淋巴细胞 antigen-4 (CTLA-4 ) 在很少的病人导致变形黑瘤的调停免疫者的长期的控制。尽管 ipilimumab 无疑经由 immunostimulation 施加它的治疗学的效果,这样远的临床上有用的、 immunologically 相关的 biomarkers 预言治疗效率是逃犯的。这里,我们显示出 IL-2 的那中立化或堵住 α并且 βIL-2 受体的子单元(CD25 和 CD122,分别地) 否则在现出症状之前的潜的老鼠模型由 CTLA-4 封锁导致了,废除了 antitumor 效果和 intratumoral T 受动器对规章的房间(Tregs ) 的比率的伴随的改进,它是。CTLA-4 封锁导致了在失去了 FoxP3 表示并且在 regressing 肿瘤积累了的 IL-2-producing 受动器房间与伴随物上升表示 Lag3, ICOS, IL-10 和 Egr2 的一个镇压 CD4 + T 房间子集的减小。当 recombinant IL-2 改进了 CTLA-4 封锁的治疗学的功效时,圈套 IL-2 受体 α(IL-2Rα, sCD25 ) 禁止了 CTLA-4 的 anticancer 效果封锁。在收到 ipilimumab 的 262 个变形黑瘤病人, sCD25 的基线浆液集中代表了全面幸存的独立指示物,与预言到治疗的抵抗的高水平。总的来说,这些结果解开为在 CTLA-4 的 anticancer 活动的 IL-2 和 IL-2 受体的一个角色封锁。重要地,我们的学习提供第一 immunologically 相关的 biomarker,也就是提高的浆液 sCD25,那与黑瘤在病人预言抵抗到 CTLA-4 封锁。 | Dalil Hannani Marie Vetizou David Enot Sylvie Rusakiewicz Nathalie Chaput David Klatzmann Melanie Desbois Nicolas Jacquelot Nadege Vimond Salem Chouaib Christine Mateus James P Allison Antoni Ribas Jedd D Wolchok Jianda Yuan Philip Wong Michael Postow Andrzej Mackiewicz Jacek Mackiewicz Dirk Schadendorff Dirk Jaeger Alan J Korman Keith Bahjat Michele Maio Luana Calabro Michele WL Teng Mark J Smyth Alexander Eggennont Caroline Robert Guido Kroemer Laurence Zitvogel | 2015 | Cell Research2015，25，2： | 14 |
| 6 | MLKL regulates necrotic plasma membrane permeabilization显示文摘 | Lorenzo Galluzzi | 2014 | Cell Research2014，24，2： | 12 |
| 7 | Autophagy in the Pathogenesis of Disease显示文摘 | Beth Levine Guido Kroemer | 2008 | Cell2008，，1： | 8 |
| 8 | Sustained Type I interferon signaling as a mechanism of resistance to PD-1 blockade显示文摘PD-1 blockade represents a major therapeutic avenue in anticancer immunotherapy.Delineating mechanisms of secondary resistance to this strategy is increasingly important.Here,we identified the deleterious role of signaling via the type I interferon(IFN)receptor in tumor and antigen presenting cells,that induced the expression of nitric oxide synthase 2(N0S2),associated with intratumor accumulation of regulatory T cells(Treg)and myeloid cells and acquired resistance to anti-PD-1 monoclonal antibody(mAb).Sustained IFNP transcription was observed in resistant tumors,in turn inducing PD-L1 and N0S2 expression in both tumor and dendritic cells(DC).Whereas PD-L1 was not involved in secondary resistance to anti-PD-1 mAb,pharmacological or genetic inhibition of N0S2 maintained long-term control of tumors by PD-1 blockade,through reduction of Treg and DC activation.Resistance to immunotherapies,including anti-PD-1 mAb in melanoma patients,was also correlated with the induction of a type I IFN signature.Hence,the role of type I IFN in response to PD-1 blockade should be revisited as sustained type I IFN signaling may contribute to resistance to therapy. | Nicolas Jacquelot Takahiro Yamazaki Maria PRoberti Connie PMDuong Miles CAndrews Loic Verlingue Gladys Ferrere Sonia Becharef Marie Vetizou Romain Daillere Meriem Messaoudene David PEnot Gautier Stoll Stefano Ugel Maria Marigo Shin Foong Ngiow Aurelien Marabelle Armelle Prevost-Blondel Pierre-Olivier Gaudreau Vancheswaran Gopalakrishnan Alexander MEggermont Paule Opolon Christophe Klein Gabriele Madonna Paolo AAscierto Antje Sucker Dirk Schadendorf Mark JSm yth Jean-Charles Soria Guido Kroemer Vincenzo Bronte Jennifer Wargo and Laurence Zitvogel | 2019 | Cell Research2019，29，10： | 6 |
| 9 | The Hallmarks of Aging显示文摘 | Carlos López-Otín Maria A. Blasco Linda Partridge Manuel Serrano Guido Kroemer | 2013 | Cell2013，，6： | 5 |
| 10 | Inosine: novel microbiota-derived immunostimulatory metabolite显示文摘In a recent paper published in Science,Mager et al.identify inosine as a metabolite produced by Bifidobacterium pseudolongum that improves the efficacy of anticancer immunotherapy in mice.Inosine produced in the gut reaches adenosine A2A receptors of T lymphocytes infiltrating tumors;thus,inosine joins an expanding list of immunostimulatory metabolites produced in the gut. | Guido Kroemer Laurence Zitvogel | 2020 | Cell Research2020，30，11： | 4 |
| 11 | Mechanisms of p53-mediated mitochondrial membrane permeabilization显示文摘 | Eugenia Morselli | 2008 | Cell Research2008，18，7： | 3 |
| 12 | Autophagy and the Integrated Stress Response显示文摘 | Guido Kroemer Guillermo Mari?o Beth Levine | 2010 | Molecular Cell2010，，2： | 3 |
| 13 | IMMP2L: a mitochondrial protease suppressing cellular senescence显示文摘 | Valentina Sica Guido Kroemer | 2018 | Cell Research2018，28，6： | 2 |
| 14 | Severe COVID-19 patients exhibit an ILC2 NKG2D^(+) population in their impaired ILC compartment显示文摘Severe acute respiratory syndrome coronavirus 2(SARS-CoV-2)is responsible for the current COVID-19 disease pandemic.In some patients,the symptoms are mild,and a fraction of SARS-CoV-2-infected individuals develop severe illness with a high fatality rate due to lung damage and acute respiratory distress syndrome.1 Innate lymphoid cells(ILCs)are a recently identified type of effector immune cells that rapidly sense environmental stimuli and participate in early immune responses by promptly secreting large amounts of cytokines.2 The ILC2 subpopulation was shown to mediate Type 2 responses and to recruit eosinophils during viral lung infections upon the release of alarmins(e.g.,IL-33)by damaged epithelial cells.3,4,5 ILC2s were also shown to participate in the termination of inflammatory responses and tissue repair by amphiregulin secretion.In addition,ILC2s are critical in the early phases of allergic lung inflammation,including that induced by the protease allergen papain.6 Based on the essential function of the papain-like protease PLpro in regulating SARS-CoV-27(Fig.1a)and the severe lung damage caused by this virus,we sought to investigate the potential involvement of ILC2s in immune responses to COVID-19. | Alejandra Gomez-Cadena Laurie Spehner Marie Kroemer Myriam Ben Khelil Kevin Bouiller Grégory Verdeil Sara Trabanelli Christophe Borg Romain Loyon Camilla Jandus | 2021 | Cellular & Molecular Immunology2021，18，2： | 2 |
| 15 | 新转化膜在汽车行业内的应用近况显示文摘过去60年间,化学公司一直为汽车制造商提供最先进的磷酸锌转化膜,若将该转化膜适当地用于金属表面,可增强漆膜的附着力和防腐蚀性。磷酸盐转化膜在过去几年中经历了多次变革,目前,该转化膜的一些主要成分及副产品在新的环境政策下受到更加严格的控制,金属及其处理行业现在面临着将传统的磷酸锌膜替换为新一代产品的挑战。本文将介绍新一代氧化锆转化膜的优势,并讨论其性能和工艺成本的节省情况。过去数年内,该技术获得了极大进展,2007年几条新转化膜商业生产线已经开始试运行。文中还将展示这些试行生产线的成果,并讨论该技术的未来发展。 | Terrence R.Giles Bruce H.Goodreau William E.Fristad Jens Kroemer Michael Frank | 2008 | 汽车工艺与材料2008，，11： | 2 |
| 16 | Entosis, a key player in cancer cell competition显示文摘 | Guido Kroemer | 2014 | Cell Research2014，24，11： | 2 |
| 17 | Right Portal Vein Ligation Combined With In Situ Splitting Induces Rapid Left Lateral Liver Lobe Hypertrophy Enabling 2-Staged Extended Right Hepatic Resection in Small-for-Size Settings显示文摘 | Andreas A. Schnitzbauer Sven A. Lang Holger Goessmann Silvio Nadalin Janine Baumgart Stefan A. Farkas Stefan Fichtner-Feigl Thomas Lorf Armin Goralcyk Rüdiger H?rbelt Alexander Kroemer Martin Loss Petra Rümmele Marcus N. Scherer Winfried Padberg Alfred K? | 2012 | Annals of Surgery2012，，3： | 2 |
| 18 | Immunogenic Cell Death in Cancer Therapy显示文摘 | Guido Kroemer Lorenzo Galluzzi Oliver Kepp Laurence Zitvogel | 2013 | Annual Review of Immunology2013，，： | 2 |
| 19 | Mechanism of Action of Conventional and Targeted Anticancer Therapies: Reinstating Immunosurveillance显示文摘 | Laurence Zitvogel Lorenzo Galluzzi Mark J. Smyth Guido Kroemer | 2013 | Immunity2013，，1： | 2 |
| 20 | Mitochondrial control of apoptosis显示文摘 | Kroemer G Zamzami N Susin S A | 1997 | Immunol Today1997，18，1： | 2 |
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