ReviewInternational immunopharmacology2008
Assembly, activation, and physiologic influence of the plasma kallikrein/kinin system.
Review in International immunopharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 85 citations in OpenAlex.
- In response to bacteria, neutrophils release extracellular vesicles capable of initiating thrombin generation through DNA-dependent and independent pathways.Journal of leukocyte biology · 2024Article
- Clinical complications in envenoming byFrontiers in immunology · 2024Review
- Targeting the contact system in a rabbit model of extracorporeal membrane oxygenation.Blood advances · 2023Article
- 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
- Kininogen supports inflammation and bacterial spreading during Streptococccus Pyogenes Sepsis.EBioMedicine · 2020Article
- Plasma kallikrein modulates immune cell trafficking during neuroinflammation via PAR2 and bradykinin release.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Limited role of kininogen in the host response during gram-negative pneumonia-derived sepsis.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Impact of Bradykinin Generation During Thrombolysis in Ischemic Stroke.Frontiers in medicine · 2018Review
- A kallikrein-targeting RNA aptamer inhibits the intrinsic pathway of coagulation and reduces bradykinin release.Journal of thrombosis and haemostasis : JTH · 2017Article
- The initiation and effects of plasma contact activation: an overview.International journal of hematology · 2017Review
- Blood coagulation factor XII drives adaptive immunity during neuroinflammation via CD87-mediated modulation of dendritic cells.Nature communications · 2016Article
- Polyphosphate as modulator of hemostasis, thrombosis, and inflammation.Journal of thrombosis and haemostasis : JTH · 2015Review
- How it all starts: Initiation of the clotting cascade.Critical reviews in biochemistry and molecular biology · 2015Review
- Pathophysiology of Hereditary Angioedema.Pediatric allergy, immunology, and pulmonology · 2014Review
- The arrestin-selective angiotensin AT1 receptor agonist [Sar1,Ile4,Ile8]-AngII negatively regulates bradykinin B2 receptor signaling via AT1-B2 receptor heterodimers.The Journal of biological chemistry · 2013Article
- Endothelial cell permeability during hantavirus infection involves factor XII-dependent increased activation of the kallikrein-kinin system.PLoS pathogens · 2013Article
- Review
- Thrombin and vascular inflammation.Molecular and cellular biochemistry · 2012Review
- Modulation of C1-Inhibitor and Plasma Kallikrein Activities by Type IV Collagen.International journal of biomaterials · 2012Article
- Activation of the contact system at the surface of Fusobacterium necrophorum represents a possible virulence mechanism in Lemièrre's syndrome.Infection and immunity · 2011Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
The plasma kallikrein/kinin system that consists of the proteins factor XII, prekallikrein, and high molecular weight kininogen was first recognized as a surface-activated coagulation system arising when blood or plasma interacts with artificial surfaces. Although surface-activated contact activation occurs in vivo when various negatively charged surfaces become exposed, including a developing platelet thrombus, a physiologic, non-injury mechanism for activation, regulation, and function of this system has been elusive. Recent investigations have shown that there is a physiologic pathway for assembly and activation of this system independent of factor XII. Gene deficient mice of the bradykinin B2 receptor and factor XII have been recognized to have reduced risk for arterial thrombosis. This plasma proteolytic system influences arterial thrombosis independent of influencing hemostasis. Thus, the plasma kallikrein/kinin system has two mechanisms for its activation: one that is dependent and another independent of factor XII. Better understanding of this system may lead to insight into mechanisms for arterial thrombosis, independent of hemostasis.
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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.