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Ferroptosis: A Promising Therapeutic Target for Neonatal Hypoxic-Ischemic Brain Injury
Eric S Peeples1,2,3, Thiago C Genaro-Mattos3,4
1Department of Pediatrics, University of Nebraska Medical Center, Omaha, NE 68198, USA.
Insights
Ferroptosis, a cell death pathway involving lipid peroxidation, is increasingly recognized as a key factor in neonatal hypoxic-ischemic brain injury (HIBI). Understanding ferroptosis pathways and interventions is crucial for treating HIBI.
Area of Science:
- Neuroscience
- Cell Biology
- Pathology
Background:
- Ferroptosis is programmed cell death driven by phospholipid peroxidation.
- It is implicated in diseases involving ischemic-reperfusion injury.
- Ferroptosis is a potential key mechanism in neonatal hypoxic-ischemic brain injury (HIBI).
Purpose of the Study:
- To review ferroptotic pathways in the context of neonatal HIBI.
- To explore the activation mechanisms of ferroptosis following HIBI.
- To identify interventions that may reduce ferroptotic cell death in HIBI.
Main Methods:
- Literature review of ferroptosis and HIBI.
- Analysis of cellular pathways involved in ferroptosis.
- Examination of current and investigational therapeutic strategies.
Main Results:
- Ferroptosis pathways can be activated by HIBI.
- Specific molecular mechanisms link HIBI to ferroptosis.
- Several interventions show potential to mitigate ferroptosis in HIBI models.
Conclusions:
- Ferroptosis is a significant contributor to neonatal brain injury.
- Targeting ferroptosis pathways offers a promising therapeutic avenue for HIBI.
- Further research is needed to translate these findings into clinical practice.
Abstract:
Ferroptosis is a type of programmed cell death caused by phospholipid peroxidation that has been implicated as a mechanism in several diseases resulting from ischemic-reperfusion injury. Most recently, ferroptosis has been identified as a possible key injury mechanism in neonatal hypoxic-ischemic brain injury (HIBI). This review summarizes the current literature regarding the different ferroptotic pathways, how they may be activated after neonatal HIBI, and which current or investigative interventions may attenuate ferroptotic cell death associated with neonatal HIBI.
