ArticleBlood2012
ADAMTS13 deficiency exacerbates VWF-dependent acute myocardial ischemia/reperfusion injury in mice.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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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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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.
- Association between plasma ADAMTS13 levels/activity and the risk of ischemic stroke and outcomes of recanalization therapies: a systematic review and meta-analysis.Frontiers in neurology · 2025Pooled it
- Mouse models to study von Willebrand factor in inflammation: a scoping review.Intensive care medicine experimental · 2026Review
- Identification of missense variants in the C-domains of von Willebrand factor that cause gain-of-function-like activity.Blood advances · 2026Article
- Immune and stromal remodeling underlies radiation-induced heart injury: insights from single-cell transcriptomics.Frontiers in cardiovascular medicine · 2026Article
- Beyond Direct Fibrinolysis: Novel Approaches to Thrombolysis.Pharmaceuticals (Basel, Switzerland) · 2025Review
- von Willebrand Factor Deficiency Inhibits Endothelial-to-Mesenchymal Transition to Attenuate Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
- Spatial multiomics of acute myocardial infarction reveals immune cell infiltration through the endocardium.Nature cardiovascular research · 2025Article
- An Expendable Player in Positive Vascular Remodeling? ADAMTS13 Deficiency Does Not Affect Arteriogenesis or Angiogenesis.International journal of molecular sciences · 2025Article
- Perioperative Profiling of a Disintegrin and Metalloprotease with Thrombospondin Type 1 Motif, Member 13 (ADAMTS13) Activity in Cardiac Surgery: Kinetics and Mechanistic Insights.Journal of clinical medicine · 2025Article
- To Gain Insights into the Pathophysiological Mechanisms of the Thrombo-Inflammatory Process in the Atherosclerotic Plaque.International journal of molecular sciences · 2023Review
- Regulation of von Willebrand factor by ADAMTS13 ameliorates lipopolysaccharide-induced lung injury in mice.International journal of hematology · 2023Article
- Coagulation factor VIII regulates von Willebrand factor homeostasis invivo.Journal of thrombosis and haemostasis : JTH · 2023Article
- Animal models for thrombotic thrombocytopenic purpura: a narrative review.Annals of blood · 2023Article
- Cadmium, von Willebrand factor and vascular aging.npj aging · 2023Review
- Transcriptome analysis reveals ADAMTS15 is a potential inflammation-related gene in remote ischemic postconditioning.Frontiers in cardiovascular medicine · 2023Article
- Plasma von Willebrand Factor Is Elevated Hyperacutely After Mild Traumatic Brain Injury.Neurotrauma reports · 2023Article
- Article
- Altered VWF:ADAMTS13 homeostasis is a target for therapeutic intervention in sickle cell disease.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Thromboinflammation: From Atherosclerosis to COVID-19.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Constitutively active ADAMTS13: An emerging thrombolytic agent for acute ischemic stroke.Journal of thrombosis and haemostasis : JTH · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiologic studies suggest that elevated VWF levels and reduced ADAMTS13 activity in the plasma are risk factors for myocardial infarction. However, it remains unknown whether the ADAMTS13-VWF axis plays a causal role in the pathophysiology of myocardial infarction. In the present study, we tested the hypothesis that ADAMTS13 reduces VWF-mediated acute myocardial ischemia/reperfusion (I/R) injury in mice. Infarct size, neutrophil infiltration, and myocyte apoptosis in the left ventricular area were quantified after 30 minutes of ischemia and 23.5 hours of reperfusion injury. Adamts13(-/-) mice exhibited significantly larger infarcts concordant with increased neutrophil infiltration and myocyte apoptosis compared with wild-type (WT) mice. In contrast, Vwf(-/-) mice exhibited significantly reduced infarct size, neutrophil infiltration, and myocyte apoptosis compared with WT mice, suggesting a detrimental role for VWF in myocardial I/R injury. Treating WT or Adamts13(-/-) mice with neutralizing Abs to VWF significantly reduced infarct size compared with control Ig-treated mice. Finally, myocardial I/R injury in Adamts13(-/-)/Vwf(-/-) mice was similar to that in Vwf(-/-) mice, suggesting that the exacerbated myocardial I/R injury observed in the setting of ADAMTS13 deficiency is VWF dependent. These findings reveal that ADAMTS13 and VWF are causally involved in myocardial I/R injury.
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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.