ReviewSpringer seminars in immunopathology2005
C1 inhibitor: molecular and clinical aspects.
Review in Springer seminars in immunopathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 115 citations in OpenAlex.
- Recombinant C1 inhibitor in the prevention of severe COVID-19: a randomized, open-label, multi-center phase IIa trial.Frontiers in immunology · 2023Trial
- The 2025 WAO Guidelines for the classification, diagnosis, and treatment of hereditary angioedema, with consideration of worldwide disparities.The World Allergy Organization journal · 2026Article
- Cortical Stimulation-Based Transcriptome Shifts on Parkinson's Disease Animal Model.ASN neuro · 2025Article
- Decreased serpin C1 in extracellular vesicles predicts response to methotrexate treatment in patients with pulmonary sarcoidosis.Respiratory research · 2024Article
- A branching model of lineage differentiation underpinning the neurogenic potential of enteric glia.Nature communications · 2023Article
- Article
- Antibody-Dependent Complement Responses toward SARS-CoV-2 Receptor-Binding Domain Immobilized on "Pseudovirus-like" Nanoparticles.ACS nano · 2022Article
- Association of Complement and MAPK Activation With SARS-CoV-2-Associated Myocardial Inflammation.JAMA cardiology · 2022Article
- The Mechanisms Underlying the Protective Action of Selenium Nanoparticles against Ischemia/Reoxygenation Are Mediated by the Activation of the CaInternational journal of molecular sciences · 2021Article
- Extracellular vesicle Cystatin C and CD14 are associated with both renal dysfunction and heart failure.ESC heart failure · 2020Article
- The Immunopathology of Complement Proteins and Innate Immunity in Autoimmune Disease.Clinical reviews in allergy & immunology · 2020Review
- An update on the genetics and pathogenesis of hereditary angioedema.Genes & diseases · 2020Review
- Dietary plant extracts modulate gene expression profiles in alveolar macrophages of pigs experimentally infected with porcine reproductive and respiratory syndrome virus.Journal of animal science and biotechnology · 2020Article
- KCNH2-3.1 mediates aberrant complement activation and impaired hippocampal-medial prefrontal circuitry associated with working memory deficits.Molecular psychiatry · 2020Article
- Longitudinal Stroke Recovery Associated With Dysregulation of Complement System-A Proteomics Pathway Analysis.Frontiers in neurology · 2020Article
- Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?Frontiers in immunology · 2020Article
- Hemostatic Testing in Critically Ill Infants and Children.Frontiers in pediatrics · 2020Review
- Evaluation and Management of Angioedema in the Emergency Department.The western journal of emergency medicine · 2019Review
- Gene therapy for C1 esterase inhibitor deficiency in a Murine Model of Hereditary angioedema.Allergy · 2019Article
- Transcriptome analysis reveals immune-related gene expression changes with age in giant panda (Aging · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1 inhibitor (C1-INH) is a serine protease inhibitor (serpins) that inactivates several different proteases in the complement, contact, coagulation, and fibrinolytic systems. By its C-terminal part (serpin domain), characterized by three beta-sheets and an exposed mobile reactive loop, C1-INH binds, and blocks the activity of its target proteases. The N-terminal end (nonserpin domain) confers to C1-INH the capacity to bind lipopolysaccharides and E-selectin. Owing to this moiety, C1-INH intervenes in regulation of the inflammatory reaction. The heterozygous deficiency of C1-INH results in hereditary angioedema (HAE). The clinical picture of HAE is characterized by bouts of local increase in vascular permeability. Depending on the affected site, patients suffer from disfiguring subcutaneous edema, abdominal pain, vomiting and/or diarrhoea for edema of the gastrointestinal mucosa, dysphagia, and dysphonia up to asphyxia for edema of the pharynx and larynx. Apart from its genetic deficiency, there are several pathological conditions such as ischemia-reperfusion, septic shock, capillary leak syndrome, and pancreatitis, in which C1-INH has been reported to either play a pathogenic role or be a potential therapeutic tool. These potential applications were identified long ago, but controlled studies have not been performed to confirm pilot experiences. Recombinant C1-INH, produced in transgenic animals, has recently been produced for treatment of HAE, and clinical trials are in progress. We can expect that the introduction of this new product, along with the existing plasma derivative, will renew interest in exploiting C1-INH as a therapeutic agent.
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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.