ReviewCurrent opinion in hematology2016
Antithrombotic potential of the contact activation pathway.
Review in Current opinion in hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Coagulation factor XII haploinsufficiency is protective against venous thromboembolism in a population-scale multidimensional analysis.Nature communications · 2025Article
- A snake venom-analog peptide that inhibits SARS-CoV-2 and papain-like protease displays antithrombotic activity in mice arterial thrombosis model, without interfering with bleeding time.Thrombosis journal · 2023Article
- The endogenous thrombin potential in patients with left ventricular assist device or heart transplant.Frontiers in medicine · 2023Article
- Plant Kunitz Inhibitors and Their Interaction with Proteases: Current and Potential Pharmacological Targets.International journal of molecular sciences · 2022Review
- Kallikrein directly interacts with and activates Factor IX, resulting in thrombin generation and fibrin formation independent of Factor XI.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Novel anti-thrombotic mechanisms mediated by Mas receptor as result of balanced activities between the kallikrein/kinin and the renin-angiotensin systems.Pharmacological research · 2020Review
- The rebirth of the contact pathway: a new therapeutic target.Current opinion in hematology · 2020Review
- The First Korean Case of High-Molecular-Weight Kininogen Deficiency, With a Novel Variant, c.488delG, in theAnnals of laboratory medicine · 2020Article
- Article
- Plasma contact factors as therapeutic targets.Blood reviews · 2018Review
- Inhibition of Factors XI and XII for Prevention of Thrombosis Induced by Artificial Surfaces.Seminars in thrombosis and hemostasis · 2018Review
- Heparin induced thrombocytopenia with mechanical circulatory support devices: review of the literature and management considerations.Journal of thrombosis and thrombolysis · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
purpose of reviewThis report examines the mechanism(s) by which each protein of the contact activation system - factor XII (FXII), high-molecular-weight kininogen, and prekallikrein - influences thrombosis risk. RECENT
findingsFXII generates thrombin through contact activation via interaction with artificial surfaces as on medical instruments such as indwelling catheters, mechanical valves, stents, and ventricular assist devices. Inhibition of FXIIa-mediated contact activation prevents thrombosis under contact activation circumstances without affecting hemostasis. Current studies suggest that high-molecular-weight kininogen deficiency parallels that of FXII and inhibits contact activation. Prekallikrein inhibition contributes to thrombosis prevention by contact activation inhibition in the nylon monofilament model of transient middle cerebral artery occlusion. However, in arterial thrombosis models where reactive oxygen species are generated, prekallikrein deficiency results in downregulation of vessel wall tissue factor generation with reduced thrombin generation. Exploiting this latter prekallikrein pathway for thrombosis risk reduction provides a general, overall reduced tissue factor, antithrombotic pathway without risk for bleeding. SUMMARY: These investigations indicate that the proteins of the contact activation and kallikrein/kinin systems influence thrombosis risk by several mechanisms and understanding of these pathway provides insight into several novel targets to prevent thrombosis without increase in bleeding risk.
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What OpenQuestion holds
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.