ReviewImmunology letters2011
Cross-talk between the complement and the kinin system in vascular permeability.
Review in Immunology letters, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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.
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Who cites it
33 citing papers in PubMed, 78 citations in OpenAlex.
- Endothelial transmigration by Trypanosoma cruzi.PloS one · 2013Trial
- Pathogenicity and virulence of Rodent-Borne Orthohantaviruses.Virulence · 2025Review
- Kinin BPharmaceuticals (Basel, Switzerland) · 2025Article
- Impact of smoking on the complement system: a narrative review.Frontiers in immunology · 2025Review
- Pathophysiological dynamics in the contact, coagulation, and complement systems during sepsis: Potential targets for nafamostat mesilate.Journal of intensive medicine · 2024Review
- Kinin BInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Circulating Blood Prognostic Biomarker Signatures for Hemorrhagic Cerebral Cavernous Malformations (CCMs).International journal of molecular sciences · 2024Article
- Assessment of the effect of 21-day head-down bed rest on the cardiovascular system by blood protein composition.Frontiers in physiology · 2024Article
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- Crosstalk between the renin-angiotensin, complement and kallikrein-kinin systems in inflammation.Nature reviews. Immunology · 2022Review
- Indices of complement activation and coagulation changes in trauma patients.Trauma surgery & acute care open · 2022Article
- Inflammation and thrombosis in COVID-19 pathophysiology: proteinase-activated and purinergic receptors as drivers and candidate therapeutic targets.Physiological reviews · 2021Review
- Interactions amongst inflammation, renin-angiotensin-aldosterone and kallikrein-kinin systems: suggestive approaches for COVID-19 therapy.The journal of venomous animals and toxins including tropical diseases · 2021Review
- Circulating Lymphocyte Subsets Induce Secondary Infection in Acute Pancreatitis.Frontiers in cellular and infection microbiology · 2020Review
- Vascular Manifestations of COVID-19 - Thromboembolism and Microvascular Dysfunction.Frontiers in cardiovascular medicine · 2020Review
- Inflammation, immunosuppressive microenvironment and breast cancer: opportunities for cancer prevention and therapy.Annals of translational medicine · 2019Review
- Blockade of the kallikrein-kinin system reduces endothelial complement activation in vascular inflammation.EBioMedicine · 2019Article
- Article
- Transcriptomics and Immunological Analyses Reveal a Pro-Angiogenic and Anti-Inflammatory Phenotype for Decidual Endothelial Cells.International journal of molecular sciences · 2019Article
- Mannose-Binding Lectin Drives Platelet Inflammatory Phenotype and Vascular Damage After Cerebral Ischemia in Mice via IL (Interleukin)-1α.Arteriosclerosis, thrombosis, and vascular biology · 2018Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The endothelium is a continuous physical barrier that regulates coagulation and selective passage of soluble molecules and circulating cells through the vessel wall into the tissue. Due to its anatomic localization, the endothelium may establish contact with components of the complement, the kinin and the coagulation systems which are the main, though not exclusive, inducers of vascular leakage. Although the complement and the kinin systems may act independently, increasing evidence suggest that there is a crosstalk that involve different components of both systems. Activation is required for the function of the two systems which are involved in pathological conditions such as hereditary and acquired angioedema (AE) and vasculitidis. The aim of this review is to discuss the contribution of complement and kinin systems to vascular leakage and the cross-talk between the two systems in the development of AE. This clinical condition is characterized by episodic and recurrent local edema of subcutaneous and submucosal tissues and is due to inherited or acquired C1-INH deficiency. Although the pathogenesis of the swelling in patients with AE was originally thought to be mediated by C2, ample evidence indicate bradykinin (BK) as the most effective mediator even though the possibility that both the complement and the kinin-forming systems may contribute to the edema has not been completely excluded. BK induces endothelial leakage interacting with B2 receptors but other molecules may be involved in the onset and maintenance of AE. In this review we shall discuss the role of B1 receptors and gC1qR/p33 in addition to that of B2 receptors in the onset of AE attacks and the importance of these receptors as new possible molecular targets for therapy.
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