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Neutrophil extracellular traps (NETs) are web‑like structures composed of decondensed chromatin and granular proteins. Initially identified as an antimicrobial defense mechanism, NETs have now been demonstrated to be profoundly involved in the processes of sterile inflammation, thrombosis and fibrosis in cardiovascular diseases. The present review systematically delineated the interaction networks between NETs and macrophages, monocytes, endothelial cells, fibroblasts and platelets, untangling NETs as a central hub that integrates the pathological triad of inflammation, thrombosis and fibrosis. Building on this foundation, the specific mechanisms of NETs in cardiac diseases, including acute myocardial infarction, atrial fibrillation and heart failure and in vascular diseases, such as atherosclerosis, hypertension and abdominal aortic aneurysm, are elaborated. Finally, from four dimensions, NETs degradation, targeting of NETs components, inhibition of NETosis formation and indirect intervention through inflammatory metabolic pathways, the preclinical evidence and translational bottlenecks of strategies such as DNase I, histone‑neutralizing agents and PAD4 inhibitors were systematically evaluated. The present review aimed to promote the transition of NETs from a fundamental pathological hub into a targetable node for cardiovascular therapy.