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Thrombosis

Glycoprotein V exerts local control of fibrin

Nature Cardiovascular Research volume 2, pages 335–336 (2023)Cite this article

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Preserving hemostasis while preventing pathological thrombosis has been a central goal in drug development. A new way to restore hemostasis is suggested by the finding that glycoprotein V is cleaved by thrombin on activated platelets, negatively regulating clotting at sites of vascular injury.

A major physiological challenge is to keep blood flowing within vessels, but to rapidly halt this flow if there is a breach in the vascular system. This process — known as hemostasis — is a delicate balance between bleeding and clotting that requires an intricate interplay between endothelial cells, circulating platelets and coagulation factors. Pathological thrombosis occurs when the balance is skewed towards clotting. Primary hemostasis begins when platelets adhere to damaged endothelia via extracellular collagen and von Willebrand factor at a site of vascular damage. Secondary hemostasis is initiated when exposed tissue factor on the subendothelium sparks activation of the coagulation cascade and generation of thrombin on the surface of activated platelets and endothelial cells. Once generated, thrombin directly activates platelets and endothelial cells, and converts fibrinogen to fibrin. Crosslinked fibrin fibers form a network around activated platelets to stabilize a growing clot.

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Authors and Affiliations

  1. Department of Pharmacology, Case Western Reserve University, Cleveland, OH, USA

    Elizabeth A. Knauss & Marvin T. Nieman

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  1. Elizabeth A. Knauss
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  2. Marvin T. Nieman
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Correspondence to Marvin T. Nieman.

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The authors have no competing interests.

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Knauss, E.A., Nieman, M.T. Glycoprotein V exerts local control of fibrin. Nat Cardiovasc Res 2, 335–336 (2023). https://doi.org/10.1038/s44161-023-00261-7

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