Abstract

Vasculogenesis is essential for embryonic development. The vasculature and the intravascular blood compartment develop in a close spatial and temporal relationship. Here we discuss how thrombin, as the common final effector of the blood coagulation system, helps to coordinate vasculogenesis. Mouse models lacking coagulation factors result in impaired thrombin generation and display a phenotype of disturbed vasculogenesis. Notably, either impaired thrombin binding to its cellular receptor PAR1 or disrupted downstream signaling via G-proteins results in very similar phenotypes in mouse models. Given that vasculogenesis in adults follows comparable signaling patterns as vasculogenesis in embryos, understanding these pathways allows the possibility of identifying potential therapeutic targets for the use in the treatment of cardiovascular disease.

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