Inflammatory responses driven by neutrophil extracellular traps in cardiovascular diseases: molecular mechanisms, emerging biomarkers, and therapeutic targets.

Cardiovascular disease (CVD) remains the leading cause of mortality and disability worldwide, characterized by high incidence, morbidity, and mortality. Although guideline-directed medical therapy has improved clinical outcomes and slowed disease progression to some extent, a substantial residual risk persists, and the progression of CVD has not been fundamentally halted. Beyond traditional risk factors such as hypertension, diabetes mellitus, and dyslipidemia, dysregulated inflammatory responses are now recognized as a central driver of CVD initiation, progression, and adverse outcomes. Neutrophil extracellular traps (NETs), as key effectors of innate immunity, contribute to inflammatory cascades through mechanisms including inflammasome activation, modulation of immune responses, and promotion of thrombosis. Accumulating evidence indicates that NETs play a critical role in a spectrum of cardiovascular conditions, including atherosclerosis, myocardial infarction, and heart failure, and are closely associated with poor prognosis. This review systematically summarizes the mechanisms by which NETs mediate inflammatory responses in CVD and discusses their roles across different disease contexts. It further explores the potential of NETs as inflammation-related biomarkers and therapeutic targets, with the aim of providing new insights into inflammation-based strategies for the prevention and treatment of CVD.