Format

Send to

Choose Destination
Mol Cell. 2017 Mar 16;65(6):965-973. doi: 10.1016/j.molcel.2017.02.024.

An Inflammatory Perspective on Necroptosis.

Author information

1
Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin 2, Ireland.
2
Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin 2, Ireland. Electronic address: martinsj@tcd.ie.

Abstract

Necroptosis (programmed necrosis) occurs in response to TNF, Fas, or TRAIL, as well as certain TLR ligands, when caspase activity required for apoptosis is blocked. Necroptosis is typically considered a highly pro-inflammatory mode of cell death, due to release of intracellular "danger signals" that promote inflammation. However, because most pro-necroptotic stimuli are intrinsically highly pro-inflammatory-due to their ability to initiate the synthesis of numerous cytokines and chemokines-the inflammatory consequences of necroptosis are complex. Here, we suggest that necroptosis might have anti-inflammatory effects in certain settings, through curbing excessive TNF- or TLR-induced inflammatory cytokine production.

KEYWORDS:

apoptosis; cell death; damage-associated molecular patterns; danger; inflammation; necroptosis; necrosis; programmed cell death

PMID:
28306512
DOI:
10.1016/j.molcel.2017.02.024
[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center