RIP3: a molecular switch for necrosis and inflammation.
TLDR
The current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases is reviewed.Abstract:
The receptor-interacting protein kinase 3 (RIP3/RIPK3) has emerged as a critical regulator of programmed necrosis/ necroptosis, an inflammatory form of cell death with important functions in pathogen-induced and sterile inflammation. RIP3 activation is tightly regulated by phosphorylation, ubiquitination, and caspase-mediated cleavage. These post-translational modifications coordinately regulate the assembly of a macromolecular signaling complex termed the necrosome. Recently, several reports indicate that RIP3 can promote inflammation independent of its pronecrotic activity. Here, we review our current understanding of the mechanisms that drive RIP3-dependent necrosis and its role in different inflammatory diseases.read more
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Necroptosis in Nonalcoholic Steatohepatitis.
TL;DR: It is demonstrated that mice deficient for Rip3 show a clear reduction in MCD-diet-induced liver injury, inflammation, and liver fibrosis compared with wild-type mice, and this finding is consistent with a previous study showing similar protective effects of Rip3-deletion in a mouse model of alcoholic steatohepatitis.
Journal ArticleDOI
Cholangiocyte death in ductopenic cholestatic cholangiopathies: Mechanistic basis and emerging therapeutic strategies
Soraya Salas-Silva,Arturo Simoni-Nieves,Jocelyn Lopez-Ramirez,Leticia Bucio,Luis Enrique Gómez-Quiroz,Luis Enrique Gómez-Quiroz,María Concepción Gutiérrez-Ruiz,María Concepción Gutiérrez-Ruiz,Marcelo G. Roma +8 more
TL;DR: This review summarizes the features of the more common ductopenic syndromes and the cellular mechanisms involved in cholengiocellular death, with focus on the main forms of cholangiocyte death described so far, namely apoptosis, autophagy, necrosis, and necroptosis.
Journal ArticleDOI
Necrosulfonamide Attenuates Spinal Cord Injury via Necroptosis Inhibition.
TL;DR: Research indicates NSA attenuates the spinal cord injury via necroptosis inhibition and might be a potential and safe chemical benefit for SCI therapy.
Journal ArticleDOI
A receptor-interacting protein 1 (RIP1)-independent necrotic death under the control of protein phosphatase PP2A that involves the reorganization of actin cytoskeleton and the action of cofilin-1.
TL;DR: G5, a non-selective isopeptidase inhibitor, triggers a distinct necrotic pathway that depends on the protein phosphatase PP2A and the actin cytoskeleton that is defined by the existence of two distinct Necrotic pathways.
Journal ArticleDOI
The role of RIP3 in cardiomyocyte necrosis induced by mitochondrial damage of myocardial ischemia–reperfusion
Huifang Hou,Huifang Hou,Yongling Wang,Qiong Li,Zaibing Li,Yan Teng,Jingyu Li,Xiaoying Wang,Junli Chen,Ning Huang +9 more
TL;DR: The results showed that H/R could cause RIP3-depended mitochondrial fragmentation and necrosis-based death; andRIP3-promoted H/ R-induced necroptosis in H9c2 cells through increasing lactate dehydrogenase release and inhibiting cell viability.
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