Role of neutrophil extracellular traps in myocardial infarction pathogenesis, diagnosis, and treatment

Cardiovascular Diseases (CVDs) still reign as the leading cause of mortality worldwide, with Myocardial Infarction (MI) being one of the most life-threatening manifestations. Mounting evidence highlights the critical role of inflammation, specifically neutrophil activity, in MI pathogenesis, progression, resolution, and complications. Neutrophil Extracellular Traps (NETs), originally thought of only as antimicrobial defense mechanisms, have become widely accepted as key mediators of thrombo-inflammation, plaque rupture, microvascular obstruction, and maladaptive cardiac remodeling following an MI. This narrative review explores the multifaceted involvement of NETosis in MI, from its role in atherosclerotic plaque instability and thrombus formation to its influence on reperfusion injury and development of heart failure. Additionally, the use of circulating NET markers as potential diagnostic markers of MIs is discussed, along with novel therapeutic strategies aimed at modulating NET formation or promoting their clearance in an effort to treat MIs and prevent NET-mediated complications. Collectively, current evidence highlights NETs as both drivers of myocardial injury and as promising targets for therapeutic interventions in MI-patients.