ArticleProceedings of the National Academy of Sciences of the United States of America2019
An antibody against HK blocks Alzheimer's disease peptide β-amyloid-induced bradykinin release in human plasma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- An antibody targeting high-molecular-weight kininogen blocks contact system activation in a model of polymicrobial sepsis.Journal of thrombosis and haemostasis : JTH · 2025Article
- Review
- Bat-derived oligopeptide LE6 inhibits the contact-kinin pathway and harbors anti-thromboinflammation and stroke potential.Zoological research · 2024Article
- Anti-HK antibody inhibits the plasma contact system by blocking prekallikrein and factor XI activation in vivo.Blood advances · 2023Article
- Vascular Dysfunction in Alzheimer's Disease: Alterations in the Plasma Contact and Fibrinolytic Systems.International journal of molecular sciences · 2023Review
- Angiotensin II Receptor Blockers Reduce Tau/Aß42 Ratio: A Cerebrospinal Fluid Biomarkers' Case-Control Study.Pharmaceutics · 2023Article
- Anti-HK antibody reveals critical roles of a 20-residue HK region for Aβ-induced plasma contact system activation.Blood advances · 2022Article
- Advances in aptamers against Aβ and applications in Aβ detection and regulation for Alzheimer's disease.Theranostics · 2022Review
- The contact activation system and vascular factors as alternative targets for Alzheimer's disease therapy.Research and practice in thrombosis and haemostasis · 2021Article
- Plasma contact factors as novel biomarkers for diagnosing Alzheimer's disease.Biomarker research · 2021Article
- Increased Contact System Activation in Mild Cognitive Impairment Patients with Impaired Short-Term Memory.Journal of Alzheimer's disease : JAD · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Bradykinin is a proinflammatory factor that mediates angioedema and inflammation in many diseases. It is a key player in some types of hereditary angioedema and is involved in septic shock, traumatic injury, Alzheimer's disease (AD), and stroke, among others. Activation of the plasma contact system leads to elevated levels of plasma kallikrein, which cleaves high molecular weight kininogen (HK) to release bradykinin. Drug development for bradykinin-meditated pathologies has focused on designing inhibitors to the enzymes that cleave HK (to prevent bradykinin release) or antagonists of endothelial bradykinin receptors (to prevent downstream bradykinin action). Here we show a strategy to block bradykinin generation by using an HK antibody that binds to HK, preventing its cleavage and subsequent bradykinin release. We show that this antibody blocks dextran sodium sulfate-induced HK cleavage and bradykinin production. Moreover, while the pathogenic AD peptide β-amyloid (Aβ)42 cleaves HK and induces a dramatic increase in bradykinin production, our HK antibody blocked these events from occurring. These results may provide strategies for developing treatments for bradykinin-driven pathologies.
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