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Updated: Aug 10, 2026

A Microfluidic Flow Chamber Model for Platelet Transfusion and Hemostasis Measures Platelet Deposition and Fibrin Formation in Real-time
Published on: February 14, 2017
Inflammatory cell participation in coagulation
1Boyer Center for Molecular Medicine, Department of Pathology, Yale University School of Medicine, New Haven, CT 06536, USA.
Vascular cells, and leukocytes in particular, have evolved a formidable machinery to initiate and amplify coagulation. Through multiple, receptor-mediated recognitions this process provides a cellular microenvironment of limited proteolytic activation that contributes to the maintenance of the hemostatic balance in vivo. However, the ability of leukocytes to generate thrombin is also a fundamental aspect of inflammatory responses, and has far-reaching implications in the pathophysiology of vascular diseases. The scope of this article is to revisit the most recent contributions to the cellular and molecular mechanisms of leukocyte-mediated coagulation, and to highlight their role in the pathogenesis of vascular injury.
Vascular cells, and leukocytes in particular, have evolved a formidable machinery to initiate and amplify coagulation. Through multiple, receptor-mediated recognitions this process provides a cellular microenvironment of limited proteolytic activation that contributes to the maintenance of the hemostatic balance in vivo. However, the ability of leukocytes to generate thrombin is also a fundamental aspect of inflammatory responses, and has far-reaching implications in the pathophysiology of vascular diseases. The scope of this article is to revisit the most recent contributions to the cellular and molecular mechanisms of leukocyte-mediated coagulation, and to highlight their role in the pathogenesis of vascular injury.
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