ArticleBlood2012
Kininogen deficiency protects from ischemic neurodegeneration in mice by reducing thrombosis, blood-brain barrier damage, and inflammation.
Article in Blood, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 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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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.
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Who cites it
77 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 citations in OpenAlex.
- The efficacy and safety of fingolimod plus standardized treatment versus standardized treatment alone for acute ischemic stroke: A systematic review and meta-analysis.Pharmacology research & perspectives · 2022Pooled it
- Fingolimod enhances the efficacy of delayed alteplase administration in acute ischemic stroke by promoting anterograde reperfusion and retrograde collateral flow.Annals of neurology · 2018Trial
- The kallikrein-kinin system modulates CD4Journal of neuroinflammation · 2026Article
- Integrative proteogenomic analyses identify plasma proteins that impact the risk of ischemic stroke.Communications medicine · 2026Article
- Article
- Aqueous carbonic anhydrase-1 overexpression and its association with cytokine profiles and macular structural changes in retinal vein occlusion-associated macular edema.Scientific reports · 2025Article
- Article
- Triiodothyronine treatment in mice improves stroke outcome and reduces blood-brain barrier damage.European thyroid journal · 2025Article
- A novel nomogram based on the patient's clinical data and CT signs to predict poor outcomes in AIS patients.PeerJ · 2025Article
- Significance of Neurotransmitters in Cerebral Ischemia: Understanding the Role of Serotonin, Dopamine, Glutamate, and GABA in Stroke Recovery and Treatment.Central nervous system agents in medicinal chemistry · 2025Review
- Kininogen enhances seizure susceptibility in mice possibly through bradykinin-induced modulation of calcium transients in glutamatergic and GABAergic neurons.Frontiers in pharmacology · 2025Article
- The temporal dynamic of bradykinin type 2 receptor effects reveals its neuroprotective role in the chronic phase of cerebral and retinal ischemic injury.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025Article
- G-Protein Signaling in Alzheimer's Disease: Spatial Expression Validation of Semi-supervised Deep Learning-Based Computational Framework.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Delayed plasma kallikrein inhibition fosters post-stroke recovery by reducing thrombo-inflammation.Journal of neuroinflammation · 2024Article
- Article
- Human serum proteomics reveals a molecular signature after one night of sleep deprivation.Sleep advances : a journal of the Sleep Research Society · 2024Article
- Effective Prevention of Arterial Thrombosis with Albumin-Thrombin Inhibitor Conjugates.Molecular pharmaceutics · 2023Article
- An HBV susceptibility variant of KNG1 modulates the therapeutic effects of interferons α and λ1 in HBV infection by promoting MAVS lysosomal degradation.EBioMedicine · 2023Article
- Thromboinflammatory challenges in stroke pathophysiology.Seminars in immunopathology · 2023Review
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
17 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 6 institutions in 3 countries.
Funding
Abstract
Thrombosis and inflammation are hallmarks of ischemic stroke still unamenable to therapeutic interventions. High-molecular-weight kininogen (KNG) is a central constituent of the contact-kinin system which represents an interface between thrombotic and inflammatory circuits and is critically involved in stroke development. Kng(-/-) mice are protected from thrombosis after artificial vessel wall injury and lack the proinflammatory mediator bradykinin. We investigated the consequences of KNG deficiency in models of ischemic stroke. Kng(-/-) mice of either sex subjected to transient middle cerebral artery occlusion developed dramatically smaller brain infarctions and less severe neurologic deficits without an increase in infarct-associated hemorrhage. This protective effect was preserved at later stages of infarction as well as in elderly mice. Targeting KNG reduced thrombus formation in ischemic vessels and improved cerebral blood flow, and reconstitution of KNG-deficient mice with human KNG or bradykinin restored clot deposition and infarct susceptibility. Moreover, mice deficient in KNG showed less severe blood-brain barrier damage and edema formation, and the local inflammatory response was reduced compared with controls. Because KNG appears to be instrumental in pathologic thrombus formation and inflammation but dispensable for hemostasis, KNG inhibition may offer a selective and safe strategy for combating stroke and other thromboembolic diseases.
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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.