Mitochondria and cell death signalling
Ella Hall-Younger1, Stephen Wg Tait1
1Cancer Research UK Scotland Institute, UK; School of Cancer Sciences, University of Glasgow, Garscube Estate, Switchback Road, Glasgow, G61 1BD, UK.
Abstract:
Mitochondria are essential organelles in the life and death of a cell. During apoptosis, mitochondrial outer membrane permeabilisation (MOMP) engages caspase activation and cell death. Under nonlethal apoptotic stress, some mitochondria undergo permeabilisation, termed minority MOMP. Nonlethal apoptotic signalling impacts processes including genome stability, senescence and innate immunity. Recent studies have shown that upon MOMP, mitochondria and consequent signalling can trigger inflammation. We discuss how this occurs, and how mitochondrial inflammation might be targeted to increase tumour immunogenicity. Finally, we highlight how mitochondria contribute to other types of cell death including pyroptosis and ferroptosis. Collectively, these studies reveal critical new insights into how mitochondria regulate cell death, highlighting that mitochondrial signals engaged under nonlethal apoptotic stress have wide-ranging biological functions.
Insights
Mitochondria play a key role in cell death. Signals from nonlethal mitochondrial outer membrane permeabilisation (MOMP) trigger inflammation and impact immunity, genome stability, and senescence.
Area of Science:
- Cell Biology
- Immunology
- Molecular Biology
Background:
- Mitochondria are vital organelles regulating cellular life and death.
- Mitochondrial outer membrane permeabilisation (MOMP) is a key event in apoptosis.
- Nonlethal apoptotic stress involving minority MOMP has broad biological implications.
Purpose of the Study:
- To explore how mitochondria signal inflammation upon MOMP.
- To discuss targeting mitochondrial inflammation for cancer immunotherapy.
- To highlight mitochondria's role in pyroptosis and ferroptosis.
Main Methods:
- Review of recent studies on MOMP and mitochondrial signaling.
- Analysis of mechanisms linking mitochondrial damage to inflammatory pathways.
- Exploration of therapeutic strategies targeting mitochondrial inflammation.
Main Results:
- Mitochondrial signaling following MOMP can initiate inflammatory responses.
- Targeting mitochondrial inflammation presents a potential strategy to enhance anti-tumor immunity.
- Mitochondria are implicated in diverse cell death modalities beyond apoptosis.
Conclusions:
- Mitochondrial signals under nonlethal apoptotic stress have extensive biological functions.
- Understanding mitochondrial roles in cell death and inflammation is crucial for therapeutic development.
- Mitochondria are central regulators of cellular fate and inflammatory processes.
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