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Ferroptosis in neutrophils
Yu-Bin Lee1, Hyeong-Wook Shin1, Sanjeeb Shrestha1
1Department of Physiology, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea.
Journal of Leukocyte Biology
|April 5, 2025
Summary
Ferroptosis, a cell death process involving iron and lipid peroxidation, significantly impacts neutrophils. Understanding its role in disease and immune regulation is key for new therapeutic strategies.
Area of Science:
- Cell Biology
- Immunology
- Biochemistry
Background:
- Ferroptosis is regulated cell death driven by iron-dependent lipid peroxidation.
- It involves intricate interactions of fatty acid, iron, and antioxidant metabolism.
- Neutrophils are particularly susceptible to ferroptosis due to their cellular composition.
Purpose of the Study:
- To review the mechanisms of ferroptosis in neutrophils.
- To explore the implications of neutrophil ferroptosis in disease pathogenesis and immune regulation.
- To identify potential therapeutic targets for ferroptosis-related conditions.
Main Methods:
- Literature review of recent studies on ferroptosis in neutrophils.
- Analysis of molecular mechanisms governing neutrophil ferroptosis susceptibility and resistance.
- Examination of neutrophil extracellular trap-mediated ferroptosis induction.
Main Results:
- Neutrophils are prone to ferroptosis, influenced by iron and polyunsaturated fatty acids.
- Hypoxia can downregulate glutathione peroxidase 4, increasing ferroptosis susceptibility in some neutrophils.
- Neutrophils can induce ferroptosis in other cells via neutrophil extracellular traps, contributing to various diseases.
Conclusions:
- Neutrophil ferroptosis is a critical factor in disease progression and immune responses.
- Dysregulated ferroptosis in neutrophils has implications for conditions like ischemia-reperfusion injury and cardiotoxicity.
- Targeting ferroptosis pathways in neutrophils offers potential for novel therapeutic interventions.

