ArticleEBioMedicine2019
Blockade of the kallikrein-kinin system reduces endothelial complement activation in vascular inflammation.
Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
22 citing papers in PubMed, 38 citations in OpenAlex.
- The Kininogen 1/bradykinin receptor B2 system serves as a key molecular response of vancomycin-induced nephrotoxicity and may be a potential target of absinthin.Histology and histopathology · 2026Article
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Cellular signaling pathway of Shiga toxin-induced ATP release.Frontiers in cellular and infection microbiology · 2026Article
- Quantitative proteomics unveils potential plasma biomarkers and provides insights into the pathophysiological mechanisms underlying equine metabolic syndrome.BMC veterinary research · 2025Article
- Bradykinin B1 receptor signaling triggers complement activation on endothelial cells.Frontiers in immunology · 2025Article
- Novel Insights into the Kallikrein-Kinin System in Fulminant Myocarditis: Physiological Basis and Potential Therapeutic Advances.Journal of inflammation research · 2024Review
- Research progress of NF-κB signaling pathway and thrombosis.Frontiers in immunology · 2023Review
- Highly Increased Levels of Inter-α-inhibitor Heavy Chain 4 (ITIH4) in Autoimmune Cholestatic Liver Diseases.Journal of clinical and translational hepatology · 2022Article
- Ameliorative Effect of Dabigatran on CFA-Induced Rheumatoid Arthritis via Modulating Kallikrein-Kinin System in Rats.International journal of molecular sciences · 2022Article
- Crosstalk between the renin-angiotensin, complement and kallikrein-kinin systems in inflammation.Nature reviews. Immunology · 2022Review
- Alteration of Serum Proteome in Levo-Thyroxine-Euthyroid Thyroidectomized Patients.Journal of clinical medicine · 2022Article
- Tissue-specific pathway activities: A retrospective analysis in COVID-19 patients.Frontiers in immunology · 2022Article
- Whole patient knowledge modeling of COVID-19 symptomatology reveals common molecular mechanisms.Frontiers in molecular medicine · 2022Article
- Tubule-mitophagic secretion of SerpinG1 reprograms macrophages to instruct anti-septic acute kidney injury efficacy of high-dose ascorbate mediated by NRF2 transactivation.International journal of biological sciences · 2022Article
- Recent advances in Extracellular Vesicles and their involvements in vasculitis.Free radical biology & medicine · 2021Review
- The SARS-CoV-2/Receptor Axis in Heart and Blood Vessels: A Crisp Update on COVID-19 Disease with Cardiovascular Complications.Viruses · 2021Review
- Pathophysiological Association of Endothelial Dysfunction with Fatal Outcome in COVID-19.International journal of molecular sciences · 2021Review
- Effect of Biologics on Cardiovascular Inflammation: Mechanistic Insights and Risk Reduction.Journal of inflammation research · 2021Review
- Endothelial activation and dysfunction in COVID-19: from basic mechanisms to potential therapeutic approaches.Signal transduction and targeted therapy · 2020Review
- Kinin B1 Receptor Is Important in the Pathogenesis of Myeloperoxidase-Specific ANCA GN.Journal of the American Society of Nephrology : JASN · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe complement and kallikrein-kinin systems (KKS) are activated during vascular inflammation. The aim of this study was to investigate if blockade of the KKS can affect complement activation on the endothelium during inflammation.
methodsComplement deposition on endothelial microvesicles was assayed in vasculitis patient plasma samples and controls. Plasma was perfused over glomerular endothelial cells and complement deposition assayed by flow cytometry. The effect of the kinin system was assessed using kinin receptor antagonists and C1-inhibitor. The in vivo effect was assessed in kidney sections from mice with nephrotoxic serum-induced glomerulonephritis treated with a kinin receptor antagonist.
findingsVasculitis patient plasma had significantly more C3- and C9-positive endothelial microvesicles than controls. Perfusion of patient acute-phase plasma samples over glomerular endothelial cells induced the release of significantly more complement-positive microvesicles, in comparison to remission or control plasma. Complement activation on endothelial microvesicles was reduced by kinin B1- and B2-receptor antagonists or by C1-inhibitor (the main inhibitor of the classical pathway and the KKS). Likewise, perfusion of glomerular endothelial cells with C1-inhibitor-depleted plasma induced the release of complement-positive microvesicles, which was significantly reduced by kinin-receptor antagonists or C1-inhibitor. Mice with nephrotoxic serum-induced glomerulonephritis exhibited significantly reduced glomerular C3 deposition when treated with a B1-receptor antagonist.
interpretationExcessive complement deposition on the endothelium will promote endothelial injury and the release of endothelial microvesicles. This study demonstrates that blockade of the KKS can reduce complement activation and thereby the inflammatory response on the endothelium.
fundingFull details are provided in the Acknowledgements/Funding section.
Indexed as
Identifiers
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.