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http://dx.doi.org/10.1161/ATVBAHA.121.316203 | DOI Listing |
J Control Release
December 2024
Eshelman Innovation, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States; Division of Chemical Biology and Medicinal Chemistry, Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599, United States. Electronic address:
Occlusive blood clots remain a significant global health challenge and result in emergencies that are main causes of death and disability worldwide. Thrombolytic agents (including tissue plasminogen activator, tPA) are the only pharmacological means to dissolve blood clots. However, these drugs have modest efficacy and severe safety concerns persist.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2024
Department of Bioengineering, University of California, Los Angeles, CA 90095.
J Thromb Haemost
January 2024
Department of Experimental Medicine, McGill University, Montreal, Quebec, Canada; Research Institute of the McGill University Health Centre, Montreal, Quebec, Canada.
Int J Hematol
December 2023
Advanced Medical Science of Thrombosis and Hemostasis, Nara Medical University, 840 Shijo-Cho, Kashihara, Nara, 634-8521, Japan.
The relationship between von Willebrand factor (VWF) and inflammation has attracted considerable attention in recent years. VWF, which is stored in the Weibel-Palade bodies (WPBs) of endothelial cells (ECs), is released from WPBs in response to inflammatory stimuli and is thought to contribute to inflammation by promoting leukocyte extravasation. In this study, lung injury model mice were produced by intratracheal injection with lipopolysaccharides.
View Article and Find Full Text PDFJ Thromb Haemost
July 2023
Department of Pharmacology, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA. Electronic address:
Background: The hemostatic plug formation at sites of vascular injury is strongly dependent on rapid platelet activation and integrin-mediated adhesion and aggregation. However, to prevent thrombotic complications, platelet aggregate formation must be a self-limiting process. The second-wave mediator adenosine diphosphate (ADP) activates platelets via Gq-coupled P2Y and Gi-coupled P2Y receptors.
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