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Necroptosis and its role in inflammation

Author

Listed:
  • Manolis Pasparakis

    (Institute for Genetics, Centre for Molecular Medicine and Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases, University of Cologne)

  • Peter Vandenabeele

    (VIB Inflammation Research Center, Ghent University, UGhent-VIB Research Building FSVM
    Ghent University
    Methusalem program, Ghent University)

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.

Suggested Citation

  • Manolis Pasparakis & Peter Vandenabeele, 2015. "Necroptosis and its role in inflammation," Nature, Nature, vol. 517(7534), pages 311-320, January.
    • Handle: RePEc:nat:nature:v:517:y:2015:i:7534:d:10.1038_nature14191
    DOI: 10.1038/nature14191
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