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Paper Details

Defects in vein valve PROX1/FOXC2 antithrombotic pathway in endothelial cells drive the hypercoagulable state induced by trauma and critical illness.
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2023
DVT, Deep venous thrombosis, Ert2Cre, FOXC2, FOXC2 del, FOXC2 gene, FoxC2, FoxC2 deficiency, FoxC2del, Human, PROX1, anticoagulant endothelial phenotype, critical illness, critically, crush and pseudofracture of a, d, d-dimer, endothelial cells, endothelial protein C receptor, fibrin, fibrinolysis, human, hypercoagulability, hypercoagulable state, hypercoagulation, liver crush injury, mice, microthrombi, microthrombosis, mouse, multiple, oscillatory stress genes, posttrauma, rhodamine, tamoxifen, thrombin, thrombomodulin, transcription factor FOXC2, trauma, valvular hypercoagulability, von Willebrand, von Willebrand's factor

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