Neutrophil extracellular traps in inflammatory cardiovascular disorders

Abstract

Neutrophils, key players of the innate immunity system, serve as primary effectors of both acute infection and sterile inflammation. Neutrophil extracellular traps (NETs) are released by neutrophils as part of their antimicrobial defense, helping to trap and eliminate pathogenic microorganisms [1]. However, over the last decade, NETs have emerged as a remarkable example of how the innate immune system shapes cardiovascular disease (CVD) [2]. Initially described as DNA webs that capture pathogens, NETs are now recognized as complex structures enriched in histones, proteases, and enzymes that extend far beyond antimicrobial defense [1]. In cardiovascular pathologies, NETs function as powerful amplifiers of vascular injury, thrombosis, and maladaptive remodeling, while also actively participating in inflammation processes associated with myocardial infarction, atrial fibrillation, and myocarditis. The increased understanding of NETs' roles in CVD raises both excitement and concern: NETs represent not only a novel mechanistic link between inflammation and cardiovascular pathology but also a potential therapeutic target whose modulation could reshape clinical outcomes.