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Mitochondria and Inflammation: Cell Death Heats Up

Esmee Vringer1,2, Stephen W G Tait1,2

  • 1Cancer Research UK, Beatson Institute, Glasgow, United Kingdom.

Frontiers in Cell and Developmental Biology
|July 19, 2019
PubMed

Insights

Mitochondrial outer membrane permeabilization (MOMP) triggers apoptosis and inflammation. Inhibiting caspases during MOMP suppresses inflammation and may prevent tumor growth, revealing mitochondria as key inflammatory hubs.

Area of Science:

  • Cell Biology
  • Immunology
  • Molecular Biology

Background:

  • Mitochondrial outer membrane permeabilization (MOMP) is a critical step in initiating apoptosis.
  • MOMP involves the release of intermembrane space proteins, such as cytochrome c, activating caspase proteases.
  • Recent findings highlight MOMP's significant pro-inflammatory roles beyond apoptosis.

Purpose of the Study:

  • To investigate the dual role of MOMP in apoptosis and inflammation.
  • To explore the mechanisms by which MOMP activates inflammatory signaling pathways.
  • To assess the therapeutic potential of modulating MOMP-induced inflammation.

Main Methods:

  • Studied MOMP-induced apoptosis and inflammation.
  • Investigated mitochondrial DNA-dependent cGAS-STING signaling.
  • Examined IAP-regulated NF-κB signaling pathways.
  • Assessed the impact of caspase inhibition on inflammation and cell death.

Main Results:

  • MOMP activates cGAS-STING signaling, leading to type I interferon responses.
  • MOMP engages NF-κB signaling through an IAP-regulated mechanism.
  • Apoptotic caspase activity suppresses mitochondrial-dependent inflammation during cell death.
  • Inhibiting caspases during MOMP promotes immunogenic cell death and inhibits tumorigenesis.

Conclusions:

  • Mitochondria act as inflammatory signaling hubs during cell death.
  • Modulating MOMP and caspase activity offers therapeutic potential for inflammatory diseases and cancer.
  • Understanding MOMP's inflammatory functions is crucial for developing novel treatment strategies.
Keywords:
NF-κBapoptosiscaspasescell deathinflammationinterferonmitochondriamtDNA

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