Programmed necrosis/necroptosis: An inflammatory form of cell death

Book Section

It was not long ago when necrosis was thought to be cell injury caused by nonspecific physical trauma. In recent years, a dedicated pathway that triggers necrosis in response to TNF-like death cytokines, certain toll-like receptors, and in response to viral pathogens was described. Signaling adaptors that contain the RIP homotypic interaction motif (RHIM), such as receptor interacting protein kinase (RIPK) 1 and RIPK3, are key inducers for this form of regulated necrosis, often referred to as programmed necrosis or necroptosis. Genetic and biochemical experiments show that RIP kinase-dependent necrosis and caspase-dependent apoptosis are intimately linked. Unlike apoptosis, necrosis tends to promote inflammation. Emerging evidence indicates that the pro-inflammatory nature of necrosis is a critical driver in a wide range of disease pathologies. In this chapter, I discuss the molecular pathway that controls necrosis and how it contributes to different inflammatory diseases.

Full Text

Duke Authors

Cited Authors

  • Chan, FKM

Published Date

  • November 1, 2014

Volume / Issue

  • 9781461493020 /

Book Title

  • Cell Death: Mechanism and Disease

Start / End Page

  • 211 - 228

International Standard Book Number 10 (ISBN-10)

  • 1461493013

International Standard Book Number 13 (ISBN-13)

  • 9781461493013

Digital Object Identifier (DOI)

  • 10.1007/978-1-4614-9302-0_10

Citation Source

  • Scopus