Book ChapterDOI
Programmed necrosis from molecules to health and disease.
Lorenzo Galluzzi,Tom Vanden Berghe,Nele Vanlangenakker,Sabrina Buettner,Tobias Eisenberg,Peter Vandenabeele,Frank Madeo,Guido Kroemer +7 more
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TLDR
In this review, the historical evolution of the concept of programmed necrosis and the molecular mechanisms that underlie necroptosis initiation and execution are described and evidence suggesting that necroPTosis represents an ancient and evolutionarily conserved cell death modality that may be targeted for drug development is provided.Abstract:
During the past decade, cell death researchers have witnessed a gradual but deep conceptual revolution: it has been unequivocally shown that necrosis, which for long had been considered as a purely accidental cell death mode, can also be induced by finely regulated signal transduction pathways In particular, when caspases are inhibited by pharmacological or genetic means, the ligation of death receptors such as the tumor necrosis factor receptor 1 (TNFR1) can lead to the assembly of a supramolecular complex containing the receptor-interacting protein kinases 1 and 3 (RIP1 and RIP3) that delivers a pronecrotic signal Such complex has recently been dubbed necrosome and mediates the execution of a specific instance of regulated necrosis, necroptosis Soon, it turned out that programmed necrosis occurs in nonmammalian model organisms and that it is implicated in human diseases including ischemia and viral infection In this review, we first describe the historical evolution of the concept of programmed necrosis and the molecular mechanisms that underlie necroptosis initiation and execution We then provide evidence suggesting that necroptosis represents an ancient and evolutionarily conserved cell death modality that may be targeted for drug developmentread more
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Journal ArticleDOI
Regulated necrosis: the expanding network of non-apoptotic cell death pathways
Tom Vanden Berghe,Andreas Linkermann,Sandrine Jouan-Lanhouet,Henning Walczak,Peter Vandenabeele +4 more
TL;DR: Elucidating how these pathways of regulated necrosis are interconnected at the molecular level should enable this process to be therapeutically targeted.
Induction of autophagy by spermidine promotes longevity
Tobias Eisenberg,Heide Knauer,Alexandra Schauer,Sabrina Büttner,Christoph Ruckenstuhl,Didac Carmona-Gutierrez,Julia Ring,Sabrina Schroeder,Christoph Magnes,Lucia Antonacci,Heike Fussi,Luiza Deszcz,Luiza Deszcz,Regina Hartl,Regina Hartl,Elisabeth Schraml,Alfredo Criollo,Evgenia Megalou,Daniela Weiskopf,Peter Laun,Gino Heeren,Michael Breitenbach,Beatrix Grubeck-Loebenstein,Eva Herker,Birthe Fahrenkrog,Kai-Uwe Fröhlich,Frank Sinner,Nektarios Tavernarakis,Nadège Minois,Nadège Minois,Nadège Minois,Guido Kroemer,Frank Madeo +32 more
TL;DR: Administration of spermidine markedly extended the lifespan of yeast, flies and worms, and human immune cells and inhibited oxidative stress in ageing mice, and found that enhanced autophagy is crucial for polyamine-induced suppression of necrosis and enhanced longevity.
Journal ArticleDOI
Autophagy and apoptosis dysfunction in neurodegenerative disorders.
Saeid Ghavami,Shahla Shojaei,Behzad Yeganeh,Sudharsana R. Ande,Jaganmohan Reddy Jangamreddy,Maryam Mehrpour,Jonas Christoffersson,Wiem Chaabane,Adel Rezaei Moghadam,Hessam H. Kashani,Mohammad Hashemi,Ali Akbar Owji,Marek J. Łos +12 more
TL;DR: In this article, the authors provide a brief introduction to autophagy and apoptosis pathways focusing on the role of mitochondria and lysosomes, and discuss different ways that autophag and apoptotic modulation may be employed for therapeutic intervention during the maintenance of neurodegenerative disorders.
Journal ArticleDOI
TNF Dually Mediates Resistance and Susceptibility to Mycobacteria via Mitochondrial Reactive Oxygen Species
TL;DR: Using the zebrafish, the cyclophilin D-inhibiting drug alisporivir and the acid sphingomyelinase-inactivating drug, desipramine, synergize to reverse susceptibility, suggesting the therapeutic potential of these orally active drugs against tuberculosis and possibly other TNF-mediated diseases.
Journal ArticleDOI
Mitophagy-dependent necroptosis contributes to the pathogenesis of COPD
Kenji Mizumura,Kenji Mizumura,Kenji Mizumura,Suzanne M. Cloonan,Suzanne M. Cloonan,Kiichi Nakahira,Kiichi Nakahira,Abhiram R. Bhashyam,Morgan Cervo,Tohru Kitada,Kimberly Glass,Caroline A. Owen,Ashfaq Mahmood,George R. Washko,Shu Hashimoto,Stefan W. Ryter,Stefan W. Ryter,Augustine M.K. Choi +17 more
TL;DR: It is demonstrated that CS causes mitochondrial dysfunction that is associated with a reduction of mitochondrial membrane potential and implicate mitophagy-dependent necroptosis in lung emphysematous changes in response to CS exposure, suggesting that this pathway is a therapeutic target for COPD.
References
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Apoptosis: a basic biological phenomenon with wide-ranging implications in tissue kinetics.
TL;DR: Apoptosis seems to be involved in cell turnover in many healthy adult tissues and is responsible for focal elimination of cells during normal embryonic development, and participates in at least some types of therapeutically induced tumour regression.
Journal ArticleDOI
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Michael T. Lin,M. Flint Beal +1 more
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Journal ArticleDOI
Mitochondrial Membrane Permeabilization in Cell Death
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Classification of cell death: recommendations of the Nomenclature Committee on Cell Death
Guido Kroemer,Guido Kroemer,Guido Kroemer,Lorenzo Galluzzi,Lorenzo Galluzzi,Lorenzo Galluzzi,Peter Vandenabeele,John M. Abrams,Emad S. Alnemri,Eric H. Baehrecke,Mikhail V. Blagosklonny,Wafik S. El-Deiry,Pierre Golstein,Pierre Golstein,Douglas R. Green,Michael O. Hengartner,Richard A. Knight,Sharad Kumar,Stuart A. Lipton,Stuart A. Lipton,Stuart A. Lipton,Walter Malorni,Gabriel Núñez,Marcus E. Peter,Juerg Tschopp,Junying Yuan,Mauro Piacentini,Boris Zhivotovsky,Gerry Melino,Gerry Melino +29 more
TL;DR: This study details the 2009 recommendations of the NCCD on the use of cell death-related terminology including ‘entosis’, ‘mitotic catastrophe”,’ ‘necrosis‚ ‘necroptosis‚’ and ‘pyroptotic’.
Journal ArticleDOI
Toll-like receptor 4-dependent contribution of the immune system to anticancer chemotherapy and radiotherapy.
Lionel Apetoh,François Ghiringhelli,Antoine Tesniere,Antoine Tesniere,Antoine Tesniere,Michel Obeid,Michel Obeid,Michel Obeid,Carla Ortiz,Carla Ortiz,Carla Ortiz,Alfredo Criollo,Alfredo Criollo,Alfredo Criollo,Grégoire Mignot,Grégoire Mignot,Grégoire Mignot,M. Chiara Maiuri,Evelyn Ullrich,Evelyn Ullrich,Evelyn Ullrich,Patrick Saulnier,Huan Yang,Sebastian Amigorena,Bernard Ryffel,Franck J. Barrat,Paul Saftig,Francis Lévi,Francis Lévi,Rosette Lidereau,Catherine Noguès,Jean-Paul Mira,Agnès Chompret,Virginie Joulin,Françoise Clavel-Chapelon,Jean Bourhis,Fabrice Andre,Suzette Delaloge,T. Tursz,Guido Kroemer,Guido Kroemer,Guido Kroemer,Laurence Zitvogel +42 more
TL;DR: A previously unrecognized pathway for the activation of tumor antigen–specific T-cell immunity that involves secretion of the high-mobility-group box 1 (HMGB1) alarmin protein by dying tumor cells and the action of HMGB1 on Toll-like receptor 4 (TLR4) expressed by dendritic cells (DCs) is described.
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Lorenzo Galluzzi,Ilio Vitale,Ilio Vitale,Ilio Vitale,John M. Abrams,Emad S. Alnemri,Eric H. Baehrecke,Mikhail V. Blagosklonny,Ted M. Dawson,Valina L. Dawson,Wafik S. El-Deiry,Simone Fulda,Eyal Gottlieb,Douglas R. Green,Michael O. Hengartner,Oliver Kepp,Oliver Kepp,Oliver Kepp,Richard A. Knight,Sharad Kumar,Sharad Kumar,Stuart A. Lipton,Xin Lu,Frank Madeo,Walter Malorni,Patrick Mehlen,Gabriel Núñez,Marcus E. Peter,Mauro Piacentini,David C. Rubinsztein,Yufang Shi,Hans-Uwe Simon,Peter Vandenabeele,Eileen White,Junying Yuan,Boris Zhivotovsky,Gerry Melino,Gerry Melino,Guido Kroemer +38 more