Abstract: Stroke is a major cause of death and disability worldwide, and its pathogenesis is complex, involving multiple pathological processes, such as thrombosis, ischemia-reperfusion injury, inflammatory response, and blood–brain barrier disruption. In recent years, neutrophil extracellular traps have been found to be involved in the body’s anti-infection defense and to play an important role in stroke. Studies have shown that neutrophil extracellular traps promote thrombus expansion and neuroinflammation in ischemic stroke, and they may be involved in disease progression and recovery in hemorrhagic stroke by modulating local inflammation and influencing hematoma clearance. This review systematically summarizes the evolution and mechanism of action of neutrophil extracellular traps in stroke pathology. Reactive oxygen species drive the formation of neutrophil extracellular traps 6–24 hours after cerebral infarction. At 24–48 hours, they exacerbate vascular injury and thrombosis, at 48–72 hours, they aggravate neurological injury, and after 72 hours, neutrophil extracellular traps are involved in the disruption of the blood–brain barrier and the maintenance of the inflammatory response. During stroke development, neutrophil extracellular traps are involved in multiple pathological mechanisms after cerebral infarction. They induce vascular endothelial damage, exacerbating vascular leakage and edema, injuring neurons, inducing apoptosis, promoting thrombosis, participating in reperfusion injury, and damaging the blood–brain barrier. In hemorrhagic stroke, neutrophil extracellular traps are closely associated with hematoma clearance, early brain injury, and delayed cerebral ischemia, and can be used as a biomarker to assess disease progression and efficacy. In the acute phase of stroke, neutrophil extracellular traps mainly promote injury, and in the chronic phase, they mainly promote repair. Neutrophil extracellular traps, as an important biomarker of stroke, are closely correlated with stroke severity. Additionally, neutrophil extracellular traps play an important role in atherosclerosis and intracranial venous thrombosis. Current research has confirmed that deoxyribonuclease is a key drug for degrading neutrophil extracellular traps and has shown significant therapeutic potential. Peptidyl arginine deiminase 4 inhibitors and high mobility group box 1 antagonists effectively inhibit the formation of neutrophil extracellular traps through their own unique mechanisms. Multi-targeted intervention strategies for neutrophil extracellular traps have shown broad clinical application prospects. Neutrophil extracellular traps exhibit synergistic effects with anticoagulants and thrombolytic drugs, and interventions targeting neutrophil extracellular traps can influence the efficacy of anticoagulation and thrombolytic therapy. These findings provide a theoretical basis for developing new anticoagulation and thrombolysis strategies for stroke and improving clinical outcomes for patients.

Key words: atherosclerosis, cerebral hemorrhage, cerebrovascular disorders, intracranial, sinus thrombosis, stroke, subarachnoid hemorrhage, therapeutic, thrombosis, vascular endothelium