Molecular-targeted therapy of venous thromboembolism

血小板活化受体CLEC-2与podoplanin结合，从而导致血小板活化和血栓形成。本研究探讨腺病毒介导的基因转移到静脉壁后，局部基因转移是否抑制血小板聚集和血栓形成竞争。因此，尽管需要进一步的研究，但在大鼠静脉血栓形成模型中提示了靶蛋白持续表达和抗血栓形成作用的可能性。

Platelet activation receptor CLEC-2 binds to podoplanin, thereby leading to platelet activation and thrombus formation. The present study examines whether local gene transfer suppress platelet aggregation and thrombus formation after adenovirus-mediated gene transfer to venous wall competitively. As a result, although further studies are needed, the possibility of persistent expression of target protein and antithrombotic effect were suggested in a rat model of venous thrombosis.