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Nature. 2015 Jan 15;517(7534):311-20. doi: 10.1038/nature14191.

Necroptosis and its role in inflammation.

Author information

1
Institute for Genetics, Centre for Molecular Medicine and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne, 50674 Cologne, Germany.
2
1] VIB Inflammation Research Center, Ghent University, UGhent-VIB Research Building FSVM, 9052 Ghent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, 9000 Ghent, Belgium. [3] Methusalem program, Ghent University, Technologiepark 927, B-9052 Ghent, Belgium.

Abstract

Regulated cell death has essential functions in development and in adult tissue homeostasis. Necroptosis is a newly discovered pathway of regulated necrosis that requires the proteins RIPK3 and MLKL and is induced by death receptors, interferons, toll-like receptors, intracellular RNA and DNA sensors, and probably other mediators. RIPK1 has important kinase-dependent and scaffolding functions that inhibit or trigger necroptosis and apoptosis. Mouse-model studies have revealed important functions for necroptosis in inflammation and suggested that it could be implicated in the pathogenesis of many human inflammatory diseases. We discuss the mechanisms regulating necroptosis and its potential role in inflammation and disease.

PMID:
25592536
DOI:
10.1038/nature14191
[Indexed for MEDLINE]

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