ArticleFluids and barriers of the CNS2025
Neutrophil extracellular traps aggravate blood-brain barrier disruption via ZBP1/FSP1-mediated ferroptosis after traumatic brain injury.
Article in Fluids and barriers of the CNS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Targeting Peptidylarginine Deiminases in Neurons and Astrocytes in Central Nervous System Injury-Effects of Pan-PAD Inhibitor Cl-Amidine in an Oxygen-Glucose Deprivation Model of Ischaemia (OGD/R) and LPS Stimulation In Vitro.International journal of molecular sciences · 2026Article
- Study on the Function and Mechanism of Neutrophil Extracellular Traps in Regulating Necroptosis Following Traumatic Brain Injury.Brain and behavior · 2026Article
- Review
- Ferroptosis-immune crosstalk in CNS diseases: mechanisms and translational insights.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Ferroptosis plays a crucial role in secondary brain injury following traumatic brain injury (TBI). Neutrophil extracellular traps (NETs) formation has also been implicated in secondary injury after TBI. However, the relationship between NETs, blood-brain barrier (BBB) disruption, and ferroptosis remains unclear. In this study, we found that levels of NET-related biomarkers in the plasma of TBI patients were significantly elevated and positively correlated with ICAM-1 and vWF. Moreover, inhibiting NET formation via peptidylarginine deiminase 4 (PAD4) deficiency reduced ferroptosis and BBB damage. In vitro experiments demonstrated that NETs exacerbated ferroptosis in hCMEC/D3 cells, leading to BBB disruption. Knockdown of ZBP1 and overexpression of FSP1 both reversed NETs-induced ferroptosis in endothelial cells and alleviated BBB damage. Additionally, we observed a close relationship between ZBP1 and FSP1. Collectively, our findings suggest that inhibiting NETs formation can mitigate ferroptosis and BBB damage, while targeting ZBP1 and FSP1 may offer potential therapeutic strategies for improving outcomes after TBI.
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