Abstract
Platelets, traditionally viewed as central effectors of hemostasis and thrombosis, are increasingly recognized as dynamic regulators of inflammation and neural repair. In ischemic stroke, platelets contribute to the formation and stabilization of thrombi, as well as microvascular dysfunction downstream of the initial occlusion site. In both cases, platelets engage leukocytes and endothelial cells to amplify cross talk between thrombotic and inflammatory pathways, creating stable blood clots and worsening ischemic brain injury. Paradoxically, platelets also protect the ischemic brain from excessive damage by preserving vascular stability and preventing hemorrhagic transformation. This argues against broad inhibition of platelet function in the acute setting of ischemic stroke. Advances in preclinical and translational research have revealed that selective modulation of platelet-immune pathways can enhance reperfusion, preserve the neurovascular unit, and improve outcomes without increasing bleeding risk. Moving forward, precision antiplatelet strategies integrating platelet phenotyping, pharmacogenomics, and demographic risk profiling may enable individualized therapy. Recognizing the dual hemostatic and inflammatory roles of platelets is thus essential to redefining their function as active modulators of brain injury and repair.