Programmed necrosis : from molecules to health and disease
- Author
- Lorenzo Galluzzi, Tom Vanden Berghe (UGent) , Nele Vanlangenakker (UGent) , Sabrina Buettner, Tobias Eisenberg, Peter Vandenabeele (UGent) , Frank Madeo and Guido Kroemer
- Organization
- 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 development.
- Keywords
- DOMAIN KINASE RIP, OXIDATIVE STRESS, TNF-ALPHA, FOCAL CEREBRAL-ISCHEMIA, LYSOSOMAL MEMBRANE PERMEABILIZATION, NF-KAPPA-B, APOPTOSIS-INDUCING FACTOR, MITOCHONDRIAL PERMEABILITY TRANSITION, RECEPTOR-INTERACTING PROTEIN, NECROTIC CELL-DEATH, Lipid peroxidation, ROS, TNFR, RIP1, Caspases, NOX1, Glutaminolysis
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-1917670
- MLA
- Galluzzi, Lorenzo, et al. “Programmed Necrosis : From Molecules to Health and Disease.” International Review of Cell and Molecular Biology, vol. 289, Elsevier Academic, 2011, pp. 1–35, doi:10.1016/B978-0-12-386039-2.00001-8.
- APA
- Galluzzi, L., Vanden Berghe, T., Vanlangenakker, N., Buettner, S., Eisenberg, T., Vandenabeele, P., … Kroemer, G. (2011). Programmed necrosis : from molecules to health and disease. International Review of Cell and Molecular Biology, 289, 1–35. https://doi.org/10.1016/B978-0-12-386039-2.00001-8
- Chicago author-date
- Galluzzi, Lorenzo, Tom Vanden Berghe, Nele Vanlangenakker, Sabrina Buettner, Tobias Eisenberg, Peter Vandenabeele, Frank Madeo, and Guido Kroemer. 2011. “Programmed Necrosis : From Molecules to Health and Disease.” International Review of Cell and Molecular Biology 289: 1–35. https://doi.org/10.1016/B978-0-12-386039-2.00001-8.
- Chicago author-date (all authors)
- Galluzzi, Lorenzo, Tom Vanden Berghe, Nele Vanlangenakker, Sabrina Buettner, Tobias Eisenberg, Peter Vandenabeele, Frank Madeo, and Guido Kroemer. 2011. “Programmed Necrosis : From Molecules to Health and Disease.” International Review of Cell and Molecular Biology 289: 1–35. doi:10.1016/B978-0-12-386039-2.00001-8.
- Vancouver
- 1.Galluzzi L, Vanden Berghe T, Vanlangenakker N, Buettner S, Eisenberg T, Vandenabeele P, et al. Programmed necrosis : from molecules to health and disease. International Review of Cell and Molecular Biology. 2011;289:1–35.
- IEEE
- [1]L. Galluzzi et al., “Programmed necrosis : from molecules to health and disease,” International Review of Cell and Molecular Biology, vol. 289, pp. 1–35, 2011.
@article{1917670,
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 development.}},
author = {{Galluzzi, Lorenzo and Vanden Berghe, Tom and Vanlangenakker, Nele and Buettner, Sabrina and Eisenberg, Tobias and Vandenabeele, Peter and Madeo, Frank and Kroemer, Guido}},
isbn = {{9780123860392}},
issn = {{1937-6448}},
journal = {{International Review of Cell and Molecular Biology}},
keywords = {{DOMAIN KINASE RIP,OXIDATIVE STRESS,TNF-ALPHA,FOCAL CEREBRAL-ISCHEMIA,LYSOSOMAL MEMBRANE PERMEABILIZATION,NF-KAPPA-B,APOPTOSIS-INDUCING FACTOR,MITOCHONDRIAL PERMEABILITY TRANSITION,RECEPTOR-INTERACTING PROTEIN,NECROTIC CELL-DEATH,Lipid peroxidation,ROS,TNFR,RIP1,Caspases,NOX1,Glutaminolysis}},
language = {{eng}},
pages = {{1--35}},
publisher = {{Elsevier Academic}},
title = {{Programmed necrosis : from molecules to health and disease}},
url = {{http://doi.org/10.1016/B978-0-12-386039-2.00001-8}},
volume = {{289}},
year = {{2011}},
}
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