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Many stimuli pull the necrotic trigger, an overview

Nele Vanlangenakker UGent, Tom Vanden Berghe UGent and Peter Vandenabeele UGent (2012) CELL DEATH AND DIFFERENTIATION. 19(1). p.75-86
abstract
The lab of Jurg Tschopp was the first to report on the crucial role of receptor-interacting protein kinase 1 (RIPK1) in caspase-independent cell death. Because of this pioneer finding, regulated necrosis and in particular RIPK1/RIPK3 kinase-mediated necrosis, referred to as necroptosis, has become an intensively studied form of regulated cell death. Although necrosis was identified initially as a backup cell death program when apoptosis is blocked, it is now recognized as a cellular defense mechanism against viral infections and as being critically involved in ischemia-reperfusion damage. The observation that RIPK3 ablation rescues embryonic lethality in mice deficient in caspase-8 or Fas-associated-protein-via-a-death-domain demonstrates the crucial role of this apoptotic platform in the negative control of necroptosis during development. Here, we review and discuss commonalities and differences of the increasing list of inducers of regulated necrosis ranging from cytokines, pathogen-associated molecular patterns, to several forms of physicochemical cellular stress. Since the discovery of the crucial role of RIPK1 and RIPK3 in necroptosis, these kinases have become potential therapeutic targets. The availability of new pharmacological inhibitors and transgenic models will allow us to further document the important role of this form of cell death in degenerative, inflammatory and infectious diseases.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (review)
publication status
published
subject
keyword
necroptosis, necrosis, cytokines, pathogens, TUMOR-NECROSIS-FACTOR, NF-KAPPA-B, RECEPTOR-INTERACTING PROTEIN, MITOCHONDRIAL PERMEABILITY TRANSITION, INDEPENDENT CELL-DEATH, IMMUNODEFICIENCY-VIRUS TYPE-1, APOPTOSIS-INDUCING FACTOR, DOMAIN-CONTAINING ADAPTER, TNF-R1 SIGNALING COMPLEX, INNATE IMMUNE-RESPONSE
journal title
CELL DEATH AND DIFFERENTIATION
Cell Death Differ.
volume
19
issue
1
pages
75 - 86
Web of Science type
Review
Web of Science id
000298369000011
JCR category
BIOCHEMISTRY & MOLECULAR BIOLOGY
JCR impact factor
8.371 (2012)
JCR rank
26/288 (2012)
JCR quartile
1 (2012)
ISSN
1350-9047
DOI
10.1038/cdd.2011.164
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
project
Ghent researchers on unfolded proteins in inflammatory disease (GROUP-ID)
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
1996676
handle
http://hdl.handle.net/1854/LU-1996676
date created
2012-01-19 13:54:03
date last changed
2014-05-12 10:58:31
@article{1996676,
  abstract     = {The lab of Jurg Tschopp was the first to report on the crucial role of receptor-interacting protein kinase 1 (RIPK1) in caspase-independent cell death. Because of this pioneer finding, regulated necrosis and in particular RIPK1/RIPK3 kinase-mediated necrosis, referred to as necroptosis, has become an intensively studied form of regulated cell death. Although necrosis was identified initially as a backup cell death program when apoptosis is blocked, it is now recognized as a cellular defense mechanism against viral infections and as being critically involved in ischemia-reperfusion damage. The observation that RIPK3 ablation rescues embryonic lethality in mice deficient in caspase-8 or Fas-associated-protein-via-a-death-domain demonstrates the crucial role of this apoptotic platform in the negative control of necroptosis during development. Here, we review and discuss commonalities and differences of the increasing list of inducers of regulated necrosis ranging from cytokines, pathogen-associated molecular patterns, to several forms of physicochemical cellular stress. Since the discovery of the crucial role of RIPK1 and RIPK3 in necroptosis, these kinases have become potential therapeutic targets. The availability of new pharmacological inhibitors and transgenic models will allow us to further document the important role of this form of cell death in degenerative, inflammatory and infectious diseases.},
  author       = {Vanlangenakker, Nele and Vanden Berghe, Tom and Vandenabeele, Peter},
  issn         = {1350-9047},
  journal      = {CELL DEATH AND DIFFERENTIATION},
  keyword      = {necroptosis,necrosis,cytokines,pathogens,TUMOR-NECROSIS-FACTOR,NF-KAPPA-B,RECEPTOR-INTERACTING PROTEIN,MITOCHONDRIAL PERMEABILITY TRANSITION,INDEPENDENT CELL-DEATH,IMMUNODEFICIENCY-VIRUS TYPE-1,APOPTOSIS-INDUCING FACTOR,DOMAIN-CONTAINING ADAPTER,TNF-R1 SIGNALING COMPLEX,INNATE IMMUNE-RESPONSE},
  language     = {eng},
  number       = {1},
  pages        = {75--86},
  title        = {Many stimuli pull the necrotic trigger, an overview},
  url          = {http://dx.doi.org/10.1038/cdd.2011.164},
  volume       = {19},
  year         = {2012},
}

Chicago
Vanlangenakker, Nele, Tom Vanden Berghe, and Peter Vandenabeele. 2012. “Many Stimuli Pull the Necrotic Trigger, an Overview.” Cell Death and Differentiation 19 (1): 75–86.
APA
Vanlangenakker, N., Vanden Berghe, T., & Vandenabeele, P. (2012). Many stimuli pull the necrotic trigger, an overview. CELL DEATH AND DIFFERENTIATION, 19(1), 75–86.
Vancouver
1.
Vanlangenakker N, Vanden Berghe T, Vandenabeele P. Many stimuli pull the necrotic trigger, an overview. CELL DEATH AND DIFFERENTIATION. 2012;19(1):75–86.
MLA
Vanlangenakker, Nele, Tom Vanden Berghe, and Peter Vandenabeele. “Many Stimuli Pull the Necrotic Trigger, an Overview.” CELL DEATH AND DIFFERENTIATION 19.1 (2012): 75–86. Print.