In this issue of Blood, Payne et al revealed a novel function of the platelet C–type lectin-like receptor 2 (CLEC-2)/podoplanin interaction in thromboinflammation: podoplanin expression is upregulated in the vessel wall during venous thrombosis. Venous thrombosis is prevented in the absence of CLEC-2.1 The role of platelet CLEC-2 in thromboinflammation has been previously unrecognized, because CLEC-2 plays a relatively minor role in arterial thrombosis and only a minimal role in normal hemostasis. Moreover, a CLEC-2 ligand, podoplanin is not expressed in the normal vessel wall.
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Katsue Suzuki‐Inoue (2017) studied this question.
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