Brain-derived neurotrophic factor acts as a context-dependent modulator of thrombosis, amplifying platelet activation at injury sites while exerting systemic protective effects on vascular integrity.
PURPOSE OF REVIEW: Brain-derived neurotrophic factor (BDNF), a neurotrophin associated with neuronal survival and plasticity, has emerged as a significant player in cardiovascular biology. This review examines the evidence for BDNF as a regulator of hemostasis and thrombosis, integrating experimental, clinical, and genetic data to clarify its role in platelet function and thrombotic disease. RECENT FINDINGS: Human platelets represent the largest peripheral reservoir of BDNF, releasing it upon activation by classical agonists. Once secreted, BDNF further amplifies platelet activation through a truncated isoform of the TrkB receptor via a kinase-independent signaling pathway. It also modulates clot architecture by promoting thinner, less stable fibrin networks and facilitating fibrinolysis. Paradoxically, lower circulating BDNF levels are consistently associated with greater severity of ischemic stroke and coronary artery disease, suggesting a systemic protective role. Genetic studies offer a more nuanced understanding linking BDNF to endothelial dysfunction and elevated cardiovascular risk. SUMMARY: BDNF is a context-dependent modulator of thrombosis, amplifying platelet activation at sites of injury while exerting protective effects on vascular integrity systemically. Its potential as a cardiovascular biomarker and therapeutic target warrants further investigation.
Aubin et al. (Thu,) conducted a review in Hemostasis and thrombotic risk. Brain-derived neurotrophic factor (BDNF) was evaluated. Brain-derived neurotrophic factor acts as a context-dependent modulator of thrombosis, amplifying platelet activation at injury sites while exerting systemic protective effects on vascular integrity.