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Oxeiptosis: a discreet way to respond to radicals

Pietro Scaturro1, Andreas Pichlmair2

  • 1Immunopathology of Virus Infections, Institute of Virology, Technical University of Munich, Schneckenburger Str. 8, 81675 Munich, Germany.

Current Opinion in Immunology
|October 21, 2018
PubMed

Insights

Researchers discovered oxeiptosis, a new programmed cell death pathway. This caspase-independent process, involving KEAP1, PGAM5, and AIFM1, responds to reactive oxygen species (ROS) and aids pathogen clearance.

Area of Science:

  • Cell Biology
  • Immunology
  • Toxicology

Background:

  • Programmed cell death is a critical cellular response to toxins and pathogens.
  • Reactive oxygen species (ROS) are key signaling molecules in various cell death pathways.
  • Mechanisms controlling differential cellular fates based on ROS levels are not fully understood.

Purpose of the Study:

  • To investigate novel cell death pathways.
  • To elucidate the role of ROS sensing in cell death.
  • To understand the molecular mechanisms linking KEAP1, PGAM5, and AIFM1.

Main Methods:

  • Analysis of programmed cell death pathways.
  • Investigation of reactive oxygen species (ROS) signaling.
  • Identification of molecular players in cell death.

Main Results:

  • A novel caspase-independent cell death pathway, termed oxeiptosis, was identified.
  • Oxeiptosis links KEAP1's ROS sensing to PGAM5 and AIFM1.
  • Oxeiptosis is anti-inflammatory, similar to apoptosis, upon increased ROS and pathogen encounter.

Conclusions:

  • Oxeiptosis represents a distinct programmed cell death mechanism.
  • This pathway is crucial for managing cellular stress induced by ROS.
  • Oxeiptosis may play a significant role in pathogen clearance and eliminating teratogenic cells.

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