Galectin-9 drives thrombo-inflammatory circuits initiating venous thrombosis

Galectin-9 is elevated in deep vein thrombosis patients and, in Galectin-9–deficient mice, markedly impairs venous thrombus initiation by reducing platelet and neutrophil recruitment.

• Why it matters: Venous thromboembolism behaves like a thrombo-inflammatory condition, but the inflammatory-to-thrombus initiation link is not well defined.
• What they did: The study used DVT patient plasma, Galectin-9–deficient mice with inferior vena cava stenosis, intravital microscopy, microfluidics, and ex vivo platelet/neutrophil assays; Galectin-9 was also tested on TNF-/IFN-{gamma}-stimulated endothelial cells and under venous shear.
• The result: Galectin-9 neutralization partially reversed endothelial-driven platelet adhesion and fibrin(ogen) deposition, and immobilized recombinant Galectin-9 potentiated shear-dependent platelet activation and NET-rich thrombus composition, while deletion attenuated thrombus initiation without altering hemostasis.

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