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Ripoptocide - A Spark for Inflammation.

Rosalind L Ang1, Mark Chan1,2, Adrian T Ting1

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Frontiers in Cell and Developmental Biology
|August 29, 2019
PubMed
Summary
This summary is machine-generated.

Tumor Necrosis Factor (TNF) drives inflammation by triggering cell death, termed ripoptocide. Disruptions in cell death checkpoints can cause inflammatory diseases, suggesting new therapeutic targets.

Keywords:
E3 ligaseRIPK1TNFapoptosisdeubiquitinasenecroptosisripoptocideubiquitin

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Medicine

Background:

  • Tumor Necrosis Factor (TNF) is a key cytokine in inflammatory diseases like IBD, psoriasis, and RA.
  • TNF signaling activates NFκB and MAPK pathways, promoting pro-inflammatory gene expression and cell death (apoptosis/necroptosis).
  • The role of TNF-induced cell death in inflammation has been unclear, with cells typically favoring survival via two checkpoints.

Purpose of the Study:

  • To investigate the role of TNF-induced cell death in inflammation.
  • To introduce and define the term 'ripoptocide' for TNF-induced cell death.
  • To explore the potential of targeting cell death checkpoints for treating inflammatory conditions.

Main Methods:

  • Review of existing literature on TNF signaling, cell death pathways, and inflammatory diseases.
  • Analysis of molecular mechanisms governing cell death checkpoints, including RIPK1 ubiquitination and NFκB-mediated transcription.
  • Conceptual framework development for 'ripoptocide' and its link to inflammation.

Main Results:

  • Emerging data suggest TNF-induced cell death can provoke inflammation.
  • A transcription-independent checkpoint involving RIPK1 ubiquitination prevents premature cell death.
  • Disruption of this early checkpoint leads to 'ripoptocide', a form of cell death (apoptosis/necroptosis) that can be inflammatory.

Conclusions:

  • Cellular demise induced by TNF, termed ripoptocide, may be a driver of inflammation.
  • Inflammation can arise from genetic or epigenetic alterations affecting cell death checkpoint regulators.
  • Inhibiting ripoptocide by reinforcing the early checkpoint presents a potential therapeutic strategy for inflammatory diseases.