ArticleJournal of hepatology2020
Von Willebrand factor delays liver repair after acetaminophen-induced acute liver injury in mice.
Article in Journal of hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 63 citations in OpenAlex.
- Mouse models to study von Willebrand factor in inflammation: a scoping review.Intensive care medicine experimental · 2026Review
- Selenomethionine Alleviates Zearalenone-Induced Liver Injury in Rabbits Through SIRT1-FOXO1/P53 Signaling Pathway.Antioxidants (Basel, Switzerland) · 2026Article
- Mechanistic insights into hepatic cell type-specific contributions to acetaminophen-induced acute liver injury.World journal of gastroenterology · 2025Review
- Platelets mediate neutrophil infiltration and exacerbate liver injury and sinusoidal endothelial cell damage after a severe acetaminophen overdose in mice.Archives of toxicology · 2025Article
- Plasmin-mediated proteolysis of von Willebrand factor in patients with acute and chronic liver disease.Research and practice in thrombosis and haemostasis · 2025Article
- Molecular mechanisms in liver repair and regeneration: from physiology to therapeutics.Signal transduction and targeted therapy · 2025Review
- ADAMTS13 Improves Hepatic Platelet Accumulation in Pyrrolizidine Alkaloids-induced Liver Injury.Journal of clinical and translational hepatology · 2025Article
- The C3/C3aR pathway exacerbates acetaminophen-induced mouse liver injury via upregulating podoplanin on the macrophage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Novel functions for von Willebrand factor.Blood · 2024Review
- Article
- Sequential ultrasound molecular imaging for noninvasive identification and assessment of non-alcoholic steatohepatitis in mouse models.Liver research (Beijing, China) · 2023Article
- IL-33 Downregulates Hepatic Carboxylesterase 1 in Acute Liver Injury via Macrophage-derived Exosomal miR-27b-3p.Journal of clinical and translational hepatology · 2023Article
- Robust coagulation activation and coagulopathy in mice with experimental acetaminophen-induced liver failure.Journal of thrombosis and haemostasis : JTH · 2023Article
- Altered fibrinogen γ-chain cross-linking in mutant fibrinogen-γJournal of thrombosis and haemostasis : JTH · 2023Article
- Fibrin clot properties and thrombus composition in cirrhosis.Research and practice in thrombosis and haemostasis · 2023Article
- Article
- Generation of neutrophil extracellular traps in patients with acute liver failure is associated with poor outcome.Hepatology (Baltimore, Md.) · 2022Article
- The role of platelet mediated thromboinflammation in acute liver injury.Frontiers in immunology · 2022Review
- Phytochemical and antioxidant screening ofFrontiers in nutrition · 2022Article
- Mouse Models of Liver Parenchyma Injuries and Regeneration.Frontiers in cell and developmental biology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
BACKGROUND &
aimAcetaminophen (APAP)-induced acute liver failure is associated with substantial alterations in the hemostatic system. In mice, platelets accumulate in the liver after APAP overdose and appear to promote liver injury. Interestingly, patients with acute liver injury have highly elevated levels of the platelet-adhesive protein von Willebrand factor (VWF), but a mechanistic connection between VWF and progression of liver injury has not been established. We tested the hypothesis that VWF contributes directly to experimental APAP-induced acute liver injury.
methodsWild-type mice and VWF-deficient (Vwf
resultsIn wild-type mice, VWF plasma levels, high molecular weight (HMW) VWF multimers, and VWF activity decreased 24 h after APAP challenge. These changes coupled to robust hepatic VWF and platelet deposition, although VWF deficiency had minimal effect on peak hepatic platelet accumulation or liver injury. VWF plasma levels were elevated 48 h after APAP challenge, but with relative reductions in HMW multimers and VWF activity. Whereas hepatic platelet aggregates persisted in livers of APAP-challenged wild-type mice, platelets were nearly absent in Vwf
conclusionThese studies are the first to suggest a mechanistic link between VWF, hepatic platelet accumulation, and liver repair. Targeting VWF might provide a novel therapeutic approach to improve repair of the APAP-injured liver. LAY SUMMARY: Patients with acute liver injury due to acetaminophen overdose have highly elevated levels of the platelet-adhesive protein von Willebrand factor. It is not known whether von Willebrand factor plays a direct role in the progression of acute liver injury. We discovered that von Willebrand factor delays repair of the acetaminophen-injured liver in mice and that targeting von Willebrand factor, even in mice with established liver injury, accelerates liver repair.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.