Stroke remains a leading cause of disability and death worldwide, with ischemic stroke accounting for over 80% of all cases. Neutrophil extracellular traps (NETs) have emerged as key mediators of thromboinflammation, blood-brain barrier (BBB) disruption, and impaired vascular repair in stroke. NETs exacerbate BBB disruption, impede neovascularization, cause severe neurological deficits, and may adversely affect patient outcomes. NETs accumulate in stroke thrombi and perilesional brain tissue, where they may exacerbate vascular leakage, promote thrombosis, and increase the risk of tissue plasminogen activator (tPA)-associated hemorrhagic transformation. Suicidal, vital, and mitochondrial NETosis involve overlapping pathways but distinct triggers. Adenosine triphosphate (ATP)/P2X7 receptors (P2X7R), high mobility group box 1 (HMGB1), and pyruvate kinase M2 (PKM2) modulate NET formation in ischemic stroke, while heme-driven oxidative stress contributes to hemorrhagic pathology. NETs colocalize with fibrin and von Willebrand factor (vWF) in venous thrombosis, supporting their potential role as scaffolds for clot stability. In hemorrhagic stroke, NET clearance via DNase I accelerates hematoma resolution, with context-dependent effects. Pharmacological interventions – including protein-arginine deiminase 4 (PAD4) inhibitors, DNase, blockade of upstream regulators (PKM2, pyruvate dehydrogenase kinases (PDKs), cyclic GMP-AMP synthase (cGAS)-STING), and neutrophil-targeted therapies – may provide adjunctive therapeutic strategies for stroke.