ReviewPulmonary therapy2020
A Review: Does Complement or the Contact System Have a Role in Protection or Pathogenesis of COVID-19?
Review in Pulmonary therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.
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
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- COVID-19, corticosteroids and public health: a reappraisal.Public health · 2021Pooled it
- Patterns of C1-Inhibitor Plasma Levels and Kinin-Kallikrein System Activation in Relation to COVID-19 Severity.Life (Basel, Switzerland) · 2024Article
- Impaired instructive and protective barrier functions of the endothelial cell glycocalyx pericellular matrix is impacted in COVID-19 disease.Journal of cellular and molecular medicine · 2024Review
- The Contribution of Complement Protein C1q in COVID-19 and HIV Infection Comorbid with Preeclampsia: A Review.International archives of allergy and immunology · 2022Review
- How the Innate Immune System of the Blood Contributes to Systemic Pathology in COVID-19-Induced ARDS and Provides Potential Targets for Treatment.Frontiers in immunology · 2022Review
- Acute lower limb ischemia in an ICU admitted patient diagnosed with the COVID-19: A case report.Clinical case reports · 2021Article
- SARS-CoV-2 infection and thrombotic complications: a narrative review.Journal of thrombosis and thrombolysis · 2021Review
- An update: the emerging evidence of complement involvement in COVID-19.Medical microbiology and immunology · 2021Review
- The Outcome of Critically Ill COVID-19 Patients Is Linked to Thromboinflammation Dominated by the Kallikrein/Kinin System.Frontiers in immunology · 2021Observational
- Risk Factors for Mortality of COVID-19 Patient Based on Clinical Course: A Single Center Retrospective Case-Control Study.Frontiers in immunology · 2021Article
- Innate and Adaptive Immunity Alterations in Metabolic Associated Fatty Liver Disease and Its Implication in COVID-19 Severity.Frontiers in immunology · 2021Review
- Mini-Factor H Modulates Complement-Dependent IL-6 and IL-10 Release in an Immune Cell Culture (PBMC) Model: Potential Benefits Against Cytokine Storm.Frontiers in immunology · 2021Article
- Vascular Damage, Thromboinflammation, Plasmablast Activation, T-Cell Dysregulation and Pathological Histiocytic Response in Pulmonary Draining Lymph Nodes of COVID-19.Frontiers in immunology · 2021Article
- Endothelial activation and dysfunction in COVID-19: from basic mechanisms to potential therapeutic approaches.Signal transduction and targeted therapy · 2020Review
- Decreased complement C3 levels are associated with poor prognosis in patients with COVID-19: A retrospective cohort study.International immunopharmacology · 2020Observational
- Guidance for the Management of Patients with Vascular Disease or Cardiovascular Risk Factors and COVID-19: Position Paper from VAS-European Independent Foundation in Angiology/Vascular Medicine.Thrombosis and haemostasis · 2020Review
- Candesartan could ameliorate the COVID-19 cytokine storm.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2020Article
- Rationale for the use of N-acetylcysteine in both prevention and adjuvant therapy of COVID-19.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Thrombosis in Coronavirus disease 2019 (COVID-19) through the prism of Virchow's triad.Clinical rheumatology · 2020Review
- A contemporary review on pathogenesis and immunity of COVID-19 infection.Molecular biology reports · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionCOVID-19 presentation may include a profound increase in cytokines and associated pneumonia, rapidly progressing to acute respiratory distress syndrome (ARDS). This so-called cytokine storm often leads to refractory edema, respiratory arrest, and death. At present, anti-IL-6, antiviral therapy, convalescent plasma, hydroxychloroquine, and azithromycin among others are being investigated as potential treatments for COVID-19. As the disease etiology and precise therapeutic interventions are still not definitively defined, we wanted to review the roles that complement and the contact system may have in either the treatment or pathogenesis of the disease.
methodsWe searched the recent literature (PubMed) on complement and coronavirus; contact system and coronavirus; bradykinin and coronavirus; and angiotensin receptor and coronavirus. The manuscript complies with ethics guidelines and was deemed exempt from institutional review board approval according to Human Subjects Protection Office guidelines.
resultsMouse models are available for the study of coronavirus and complement. Although complement is effective in protecting against many viruses, it does not seem to be protective against coronavirus. C3 knockout mice infected with SARS-CoV had less lung disease than wild-type mice, suggesting that complement may play a role in coronavirus pathogenesis. Some evidence suggests that the observed pulmonary edema may be bradykinin-induced and could be the reason that corticosteroids, antihistamines, and other traditional interventions for edema are not effective. Angiotensin-converting enzyme 2 (ACE2) is a co-receptor for SARS-CoV-2, and studies thus far have not concluded a benefit or risk associated with the use of either ACE-inhibitors or angiotensin receptor antagonists. Activation of complement and the contact system, through generation of bradykinin, may play a role in the SARS-CoV-2-induced pulmonary edema, and our search suggests that further work is necessary to confirm our suspicions.
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Registered trials
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