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Necrosis

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
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Autophagic Cell Death

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Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
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The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

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The Intrinsic Apoptotic Pathway

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Related Experiment Video

Updated: Mar 6, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

An Inflammatory Perspective on Necroptosis.

Conor J Kearney¹, Seamus J Martin¹

¹Molecular Cell Biology Laboratory, Department of Genetics, The Smurfit Institute, Trinity College, Dublin 2, Ireland.

|March 18, 2017

Summary

This summary is machine-generated.

Necroptosis, a programmed cell death, can surprisingly reduce inflammation. This programmed necrosis may curb excessive cytokine production triggered by TNF or TLRs, offering anti-inflammatory effects in specific contexts.

Keywords:

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

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Last Updated: Mar 6, 2026

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

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Published on: August 7, 2018

Live-cell Imaging of Lysosomal Membrane Permeabilization During Necroptosis

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Published on: November 14, 2025

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

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Published on: January 20, 2023

Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

Necroptosis (programmed necrosis) is a cell death pathway activated by TNF, Fas, or TRAIL when apoptosis is inhibited.
It is generally viewed as a pro-inflammatory process due to the release of danger signals.
The inflammatory impact of necroptosis is complex, as its triggers are often inflammatory themselves.

Purpose of the Study:

To investigate the potential anti-inflammatory role of necroptosis.
To explore if necroptosis can modulate TNF- or TLR-induced inflammatory cytokine production.

Main Methods:

The study likely involved cell culture models stimulated with necroptotic inducers (e.g., TNF, specific TLR ligands).
Analysis of cytokine and chemokine production in response to these stimuli, potentially comparing necroptotic conditions with and without caspase inhibition.
Assessment of inflammatory signaling pathways.

Main Results:

Necroptosis induction was observed to potentially decrease excessive pro-inflammatory cytokine and chemokine synthesis.
This suggests a regulatory role for necroptosis in limiting inflammatory responses under certain conditions.
The findings challenge the notion of necroptosis as solely a pro-inflammatory cell death mechanism.

Conclusions:

Necroptosis may exert anti-inflammatory effects by suppressing excessive cytokine production.
This programmed necrosis pathway could serve as a counterbalance to certain inflammatory stimuli.
Understanding this duality is crucial for therapeutic strategies targeting inflammation and cell death.