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Updated: Jan 9, 2026

Author Spotlight: THP-1 Macrophage Response to LPS/ATP — Unveiling the Pyroptosis, Apoptosis, and Necroptosis Spectrum
Published on: May 3, 2024
Mitochondria in pyroptosis: Mechanisms and implications.
Basmah M Eldakhakhny1, Wesam H Abdulaal2, Johra Khan3
1Department of Clinical Biochemistry, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia; Saudi Diabetes Study Research Group, King Fahd Medical Research Centre, King Abdulaziz University, Jeddah, Saudi Arabia; Food Nutrition and Lifestyle Research Unit, King Fahd Medical Research Centre, King Abdulaziz University, Jeddah, Saudi Arabia.
Pyroptosis, a programmed cell death, involves gasdermins forming pores. Mitochondria play a key role in pyroptosis signaling, with implications for diseases like sepsis and cardiotoxicity.
Area of Science:
- Cellular Biology
- Immunology
- Molecular Medicine
Background:
- Pyroptosis is a lytic, inflammatory programmed cell death.
- It involves inflammasomes, caspases, and gasdermin pore formation.
- Gasdermins are crucial for releasing cellular contents and inflammatory mediators.
Purpose of the Study:
- To overview pyroptosis mechanisms.
- To discuss the role of mitochondria in pyroptosis.
- To explore gasdermin D-cardiolipin interaction and mitochondrial DNA signaling.
Main Methods:
- Literature review of pyroptosis mechanisms.
- Analysis of mitochondrial roles in pyroptosis.
- Discussion of emerging concepts and clinical relevance.
Main Results:
- Pyroptosis occurs via canonical (caspase-1 dependent) and non-canonical (caspase-1 independent) pathways.
- Mitochondria and mitochondrial dysfunction are critical in pre-pyroptotic signaling.
- Gasdermin D interaction with cardiolipin and mitochondrial DNA signaling are emerging areas.
Conclusions:
- Mitochondrial dysfunction is a key mediator of pyroptosis.
- Understanding these pathways offers insights into inflammatory diseases.
- Clinical relevance spans sepsis, cardiotoxicity, and other conditions.
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