ArticleExperimental and therapeutic medicine2015
Plasma von Willebrand factor level is transiently elevated in a rat model of acute myocardial infarction.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Prognostic value of plasma von Willebrand factor levels in major adverse cardiovascular events: a systematic review and meta-analysis.BMC cardiovascular disorders · 2020Pooled it
- Venous gas emboli are involved in post-dive macro, but not microvascular dysfunction.European journal of applied physiology · 2017Trial
- Time Course of Plasma Proteomic and Oxylipin Changes Induced by LPS Challenge and Modulated by Antioxidant Supplementation in a Randomized Controlled Trial.Antioxidants (Basel, Switzerland) · 2025Article
- Targeting Tumor Endothelial Cells by EGCG Using Specific Liposome Delivery System Inhibits Vascular Inflammation and Thrombosis.Cancer medicine · 2024Article
- Glycosylation changes of vWF in circulating extracellular vesicles to predict depression.Scientific reports · 2024Article
- Plasma von Willebrand factor levels in patients with cancer: A meta‑analysis.Oncology letters · 2024Article
- Palmitate Stimulates Expression of the von Willebrand Factor and Modulates Toll-like Receptors Level and Activity in Human Umbilical Vein Endothelial Cells (HUVECs).International journal of molecular sciences · 2023Article
- Cadmium, von Willebrand factor and vascular aging.npj aging · 2023Review
- Role of von Willebrand factor in the angiogenesis of lung adenocarcinoma.Oncology letters · 2022Review
- Plasma VWF: Ag levels predict long-term clinical outcomes in patients with acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
- Von Willebrand factor in diagnostics and treatment of cardiovascular disease: Recent advances and prospects.Frontiers in cardiovascular medicine · 2022Review
- Modular 3D In Vitro Artery-Mimicking Multichannel System for Recapitulating Vascular Stenosis and Inflammation.Micromachines · 2021Article
- Intracellular receptor EPAC regulates von Willebrand factor secretion from endothelial cells in a PI3K-/eNOS-dependent manner during inflammation.The Journal of biological chemistry · 2021Article
- Platelet membrane and stem cell exosome hybrid enhances cellular uptake and targeting to heart injury.Nano today · 2021Article
- Dihydroartemisinin inhibits the expression of von Willebrand factor by downregulation of transcription factor ERG in endothelial cells.Fundamental & clinical pharmacology · 2021Article
- Shear Stress-Induced Activation of von Willebrand Factor and Cardiovascular Pathology.International journal of molecular sciences · 2020Review
- Cadmium regulates von Willebrand factor and occludin expression in glomerular endothelial cells of mice in a TNF-α-dependent manner.Renal failure · 2019Article
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Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The von Willebrand factor (vWF) is a plasma glycoprotein that plays an essential role in hemostasis by supporting platelet adhesion and thrombus formation in response to vascular injury. Plasma levels of vWF are an independent risk factor for patients with acute myocardial infarction (AMI); however, clinical data have demonstrated a marked variation of vWF levels in patients with AMI, the reason for which has not yet been identified. In the present study, a rat model of ST-segment elevation AMI was established, and cardiac and peripheral blood was collected for a time-course examination of the plasma levels of vWF and tumor necrosis factor-α (TNF-α). The level of vWF in the blood plasma increased, peaked at 1 h and decreased to normal levels by day 7 following AMI, while the level of TNF-α peaked at 24 h and remained elevated until day 7. The effects of TNF-α on vWF secretion and expression were examined in cultured human umbilical vascular endothelial cells (HUVECs). TNF-α treatment increased vWF secretion from the HUVECs but inhibited the mRNA and protein expression of vWF in the HUVECs. These results indicate that vWF secretion from endothelial cells is transiently elevated following AMI, and then decreases as the expression of vWF is inhibited by TNF-α. The present study increases the understanding of the pathophysiology of vWF and indicates that the determination of vWF levels may be useful in the clinical evaluation of AMI.
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