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Updated: Nov 2, 2025
Stimulation of Vascular Endothelial Cells Using Neutrophil Extracellular Traps in the Presence of Low-Density Lipoprotein
Published on: August 12, 2025
Neutrophil extracellular traps induce thrombogenicity in severe carotid stenosis
Shihua Zhang1, Mengfan Guo2, Qianzi Liu3
1Department of Neurosurgery of the First Affiliated Hospital, Jiamusi University, Jiamusi, China.
Insights
Neutrophil extracellular traps (NETs) are elevated in symptomatic carotid stenosis patients, contributing to stroke risk. Inhibiting NETs may offer a new therapeutic target for preventing recurrent strokes.
Area of Science:
- Cardiovascular Research
- Stroke Pathophysiology
- Immunothrombosis
Background:
- Severe carotid stenosis is a major stroke risk factor.
- Symptomatic patients experience higher stroke recurrence than asymptomatic ones.
- Mechanisms driving stroke recurrence in carotid stenosis are not fully understood.
Purpose of the Study:
- To evaluate plasma neutrophil extracellular traps (NETs) levels in severe carotid stenosis.
- To investigate NETs' role in inducing procoagulant activity (PCA).
- To explore interactions between NETs, platelets, and endothelial cells (ECs).
Main Methods:
- Quantified NETs markers via ELISA.
- Detected NETting neutrophils and neutrophil-platelet aggregates using flow cytometry.
- Analyzed NETs and EC morphology with confocal microscopy.
- Assessed PCA of NETs and ECs via ELISA and fibrin formation.
Main Results:
- Symptomatic carotid stenosis patients showed significantly higher NETs levels than asymptomatic patients and healthy controls.
- Increased neutrophil-platelet aggregates correlated with NETs generation in symptomatic patients.
- NETs promoted PCA via tissue factor (TF) and disrupted the endothelial barrier, converting ECs into PCA-producing cells.
Conclusions:
- Plasma NETs levels differ between symptomatic and asymptomatic carotid stenosis patients.
- NETs are implicated in thrombogenicity in carotid stenosis.
- NETs inhibition presents a potential therapeutic strategy and biomarker for stroke prevention in severe carotid stenosis.
Background:
Severe carotid stenosis is a common cause of stroke. In addition, previous clinical studies revealed that patients symptomatic of carotid stenosis suffer from increased episodes of stroke compared with their asymptomatic counterparts. However, the mechanism underlying these differences in the recurrence of stroke remains unclear.
Objective:
The present study aimed to evaluate the levels of neutrophil extracellular traps (NETs) in the plasma of patients with severe carotid stenosis and investigate whether NETs induced procoagulant activity (PCA) in severe carotid stenosis. The study also sought to investigate the interactions between platelets or endothelial cells (ECs) and NETs.
Methods:
The levels of NETs in plasma were quantified using enzyme-linked immunosorbent assay (ELISA). In addition, NETting neutrophils and neutrophil-platelet aggregates were detected through flow cytometry. On the other hand, the morphology of NETs formation and endothelial cells were analyzed through confocal microscopy. Finally, the procoagulant activity (PCA) of NETs and endothelial cells were assessed through ELISA and fibrin formation.
Results:
Patients with symptomatic carotid stenosis patients had significantly higher levels of NETs markers compared with their asymptomatic counterparts and healthy subjects. In addition, increased levels of neutrophil-platelet aggregates induced the generation of NETs in patients with symptomatic carotid stenosis. Moreover, NETs contributed to PCA through tissue factor (TF), in patients with carotid stenosis. Furthermore, NETs disrupted the endothelial barrier and converted endothelial cells (ECs) into PCA to enhance the PCA in patients with carotid stenosis.
Conclusions:
The current study revealed differences in the levels of NETs in the plasma of symptomatic and asymptomatic patients suffering from carotid stenosis. The study also uncovered the interaction between NETs and thrombogenicity in carotid stenosis. Therefore, inhibiting NETs may be a potential biomarker and therapeutic target for recurring stroke in severe carotid stenosis.
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