Fragmented thrombi, targeted solutions: Exploring GPVI inhibition in high-shear environments

Thrombosis remains a leading cause of morbidity and mortality worldwide, particularly in the context of conditions like atherosclerosis, myocardial infarction, and ischemic stroke (1,2). Despite advancements in antiplatelet therapies, current treatments often pose significant risks of bleeding (3,4). As we strive to find more selective therapeutic targets, platelet glycoprotein (GP) VI has emerged as a potential candidate for safer, more targeted interventions.