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Updated: Feb 23, 2026
Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Placental ferroptosis in preeclampsia: An integrative and comprehensive review
Tamir Edri1, Sapir Lianski1, Sarah M Cohen1
1Obstetrics & Gynecology Division, Hadassah Medical Center, Faculty of Medicine of the Hebrew University of Jerusalem, Jerusalem, Israel.
Insights
Ferroptosis, a form of cell death involving lipid peroxidation, is increasingly linked to preeclampsia. This review explores ferroptosis
Area of Science:
- Reproductive biology and medicine
- Cellular pathology
- Biochemistry
Background:
- Preeclampsia is a significant cause of maternal and perinatal complications.
- Ferroptosis, a regulated cell death pathway, is implicated in preeclampsia's pathophysiology.
- Placental dysfunction is a key feature of preeclampsia.
Purpose of the Study:
- To review the evidence linking ferroptosis to placental dysfunction in preeclampsia.
- To explore the biochemical mechanisms underlying ferroptosis in the syncytiotrophoblast.
- To discuss the therapeutic potential of targeting ferroptosis for preeclampsia treatment.
Main Methods:
- Synthesis of current scientific literature on ferroptosis and preeclampsia.
- Detailed review of biochemical pathways involved in ferroptosis (e.g., iron metabolism, lipid peroxidation, glutathione-GPX4).
- Analysis of emerging data on systemic manifestations and therapeutic strategies.
Main Results:
- Disrupted iron metabolism, oxidative stress, and impaired antioxidant defenses promote ferroptosis in placental cells.
- Ferroptosis contributes to syncytiotrophoblast damage and placental dysfunction.
- Placental ferroptosis may drive systemic maternal complications via sFlt-1 release and endothelial injury.
Conclusions:
- Ferroptosis is a critical mechanism in preeclampsia pathogenesis.
- Targeting ferroptosis offers promising therapeutic avenues for preeclampsia.
- Ferroptosis provides a unifying framework for understanding and treating preeclampsia.
Abstract:
Ferroptosis, a regulated form of iron-dependent cell death driven by lipid peroxidation, has recently gained attention as a potential contributor to the pathophysiology of preeclampsia, a major cause of maternal and perinatal morbidity and mortality. This review synthesizes current evidence linking ferroptosis to placental dysfunction and explores its relevance to the pathogenesis of preeclampsia. We examine how disrupted iron metabolism, oxidative stress, and impaired antioxidant defenses create a permissive environment for ferroptotic damage in the syncytiotrophoblast. Key biochemical pathways, including redox phospholipid metabolism, glutathione-GPX4 activity, and mitochondrial function, are reviewed in detail. We also discuss emerging data connecting placental ferroptosis to systemic maternal manifestations via sFlt-1 release and extracellular vesicle-mediated endothelial injury. Finally, we highlight therapeutic implications, including pharmacological inhibition of ferroptosis and drug repurposing strategies. By integrating diverse mechanistic insights, ferroptosis emerges as a unifying paradigm that may reshape our understanding and treatment of preeclampsia.
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