Neutrophil extracellular traps contribute significantly to vascular dysfunction in sepsis.

Sepsis is a systemic inflammatory condition triggered by severe infection, frequently resulting in multi-organ dysfunction. Vascular dysfunction, as its core pathological mechanism, involves a vicious cycle of inflammation, coagulation, and endothelial injury. The mechanism of vascular damage caused by sepsis is widely studied, and neutrophils play a significant role in this process. Neutrophil extracellular traps (NETs) are an important mechanism. While NETs are designed to entrap pathogens, their excessive formation or impaired degradation directly drives vascular injury. NETs contribute to the exacerbation of vascular dysfunction through mechanisms including the induction of endothelial injury, the promotion of coagulation abnormalities, and the enhancement of vascular permeability. Nonetheless, the precise signaling pathways and regulatory networks governing these processes remain incompletely understood. This article seeks to systematically review the fundamental mechanisms through which NETs contribute to sepsis-associated vascular dysfunction, in addition to evaluating their potential utility as biomarkers and therapeutic targets. This review seeks to elucidate novel insights into the mechanisms underpinning vascular dysfunction in sepsis and associated clinical interventions, thereby contributing a theoretical foundation for the development of targeted therapeutic strategies to mitigate related pathophysiological damage.