ArticleTransfusion2026
Endothelial thrombomodulin-Its role in trauma-induced coagulopathy.
Article in Transfusion, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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8 authors.
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Abstract
backgroundTrauma-induced coagulopathy (TIC) describes a complex set of coagulation changes affecting severely injured patients. The thrombomodulin-protein C axis is central to the evolution of TIC. Soluble thrombomodulin (sTM) levels are elevated after injury and predict poor clinical outcomes. Recently, a heritable bleeding disorder defined by injury-related excessive bleeding, markedly elevated sTM and a THBD mutation has been described. The clinical phenotype broadly mirrors that of trauma hemorrhage, and we hypothesized that their endothelial colony forming cells (ECFCs) could be used to model trauma-induced endothelial damage. STUDY DESIGN AND
methodsOur objectives were to: (a) define the hemostatic capacity of wild type (WT-) and THBD variant (MT-) ECFCs, using global hemostatic assays, (b) determine the hemostatic changes on ECFC surfaces after exposing cells to trauma stimuli, (c) evaluate the contributions of traumatized ECFCs and trauma patient plasma to overall hemostatic capacity, to better understand the injured endothelial-coagulation interface.
resultsWe show that trauma stimuli cause significant, rapid shedding of TM from WT-cells and this reduced membrane-TM supports quicker fibrinolysis and greater thrombin generating capacity. Combining trauma plasma with traumatized ECFCs attenuates and/or negates these effects.
conclusionThis ECFC model provides novel mechanistic insights into TIC at the endothelial surface, informing future treatment strategies.
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