Feed

Neutrophil extracellular traps (NETs) have emerged as important mediators at the interface of innate immunity, thrombosis, and vascular remodeling. Aortic aneurysms and cerebrovascular diseases are now recognized as prototypical NET-driven conditions in which dysregulated immunothrombosis accelerates wall degeneration, promotes thrombus formation, and exacerbates tissue damage. This narrative review synthesizes current evidence on NET biology in the context of abdominal and thoracic aortic aneurysms, acute aortic syndromes, ischemic stroke, and intracerebral hemorrhage. First, we summarize the molecular mechanisms of NET formation, regulation, and clearance, outlining how NETs shape the immunothrombotic niche in aneurysm thrombi and the cerebral vasculature. Following this, experimental and clinical data on circulating and tissue NET markers are examined in relation to disease presence, lesion instability, hematoma expansion, and functional outcome, thereby highlighting their potential as diagnostic and prognostic biomarkers. Thereafter, pharmacological strategies that either inhibit NET formation or enhance NET degradation are discussed. We then examine how multilayered flow modulators, biodegradable scaffolds, and bioinspired stent coatings can modulate NET responses at the blood-device interface. Finally, we explore the emerging roles of multi-omics profiling, molecular imaging, artificial intelligence (AI)-based analyses in integrating NET-related signals into personalized risk prediction, device selection, and treatment monitoring. Collectively, these findings position NETs as central targets for biomarker development, immunomodulatory therapy, and immunobioengineered vascular devices. NET-informed precision management of aortic and cerebrovascular diseases is therefore a key area for further research.