Absence of receptor interacting protein kinase 3 prevents ethanol-induced liver injury
Sanjoy Roychowdhury,Megan R. McMullen,Sorana G. Pisano,Xiuli Liu,Laura E. Nagy,Laura E. Nagy +5 more
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TLDR
Ethanol‐induced hepatocyte injury is RIP3‐dependent, but independent of RIP1 kinase activity; intervention of this pathway could be targeted as a potential therapeutic strategy.About:
This article is published in Hepatology.The article was published on 2013-05-01 and is currently open access. It has received 266 citations till now. The article focuses on the topics: Necroptosis & Liver injury.read more
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Necroptosis and its role in inflammation
TL;DR: The mechanisms regulating necroptosis and its potential role in inflammation and disease are discussed and RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroPTosis and apoptosis.
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Decoding cell death signals in liver inflammation.
Catherine Brenner,Catherine Brenner,Lorenzo Galluzzi,Lorenzo Galluzzi,Oliver Kepp,Oliver Kepp,Guido Kroemer +6 more
TL;DR: The cellular and molecular mechanisms that account for the most deleterious effect of hepatic inflammation at the cellular level are discussed, that is, the initiation of a massive cell death response among hepatocytes.
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Necroptosis in development, inflammation and disease
TL;DR: The discoveries that have helped to identify the roles of RIPK1, RIPK3, MLKL and other regulators of necroptosis, and how they interact to determine cell fate are outlined.
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Cell Death and Cell Death Responses in Liver Disease: Mechanisms and Clinical Relevance
TL;DR: The clinical relevance of celldeath, focusing on biomarkers; the contribution of cell death to drug-induced, viral, and fatty liver disease and liver cancer; and evidence for cell death pathways as therapeutic targets are reviewed.
Journal ArticleDOI
CaMKII is a RIP3 substrate mediating ischemia- and oxidative stress-induced myocardial necroptosis
Ting Zhang,Yan Zhang,Mingyao Cui,Li Jin,Yimei Wang,Fengxiang Lv,Yuli Liu,Wen Zheng,Haibao Shang,Jun Zhang,Mao Zhang,Hong-Kun Wu,Jiaojiao Guo,Xiuqin Zhang,Xinli Hu,Chun-Mei Cao,Rui-Ping Xiao +16 more
TL;DR: It is shown that receptor-interacting protein 3 (RIP3) triggers myocardial necroptosis, in addition to apoptosis and inflammation, through activation of Ca2+-calmodulin–dependent protein kinase (CaMKII) rather than through the well-established RIP3 partners RIP1 and MLKL.
References
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Molecular mechanisms of necroptosis: an ordered cellular explosion.
TL;DR: Evidence now reveals that necrosis can also occur in a regulated manner, and necroptosis participates in the pathogenesis of diseases, including ischaemic injury, neurodegeneration and viral infection, thereby representing an attractive target for the avoidance of unwarranted cell death.
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Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α
TL;DR: Data indicate RIP3 as the determinant for cellular necrosis in response to TNF-alpha family of death-inducing cytokines.
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RIP3, an energy metabolism regulator that switches TNF-induced cell death from apoptosis to necrosis
TL;DR: The protein kinase receptor-interacting protein 3 (RIP3) was identified as a molecular switch between TNF-induced apoptosis and necrosis in NIH 3T3 cells and found that RIP3 was required for necrosisin other cells.
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Caspase-8 regulates TNF-α-induced epithelial necroptosis and terminal ileitis
Claudia Günther,Eva Martini,Nadine Wittkopf,Kerstin Amann,Benno Weigmann,Helmut Neumann,Maximilian J. Waldner,Stephen M. Hedrick,Stefan Tenzer,Markus F. Neurath,Christoph Becker +10 more
TL;DR: A critical function of caspase-8 is demonstrated in regulating intestinal homeostasis and in protecting IECs from TNF-α-induced necroptotic cell death and high levels of RIP3 in human Paneth cells and increased ne croptosis in the terminal ileum of patients with Crohn’s disease are identified, suggesting a potential role of necropsies in the pathogenesis of this disease.
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Necroptosis as an alternative form of programmed cell death
TL;DR: Interestingly, a death-domain containing kinase, RIP1, is involved in mediating all three pathways, with its kinase activity specifically involved in regulating necroptosis.