ReviewLife sciences2021
Preventing the development of severe COVID-19 by modifying immunothrombosis.
Review in Life sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 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
37 citing papers in PubMed, 51 citations in OpenAlex.
- Trial
- Soluble CD13 is a potential mediator of neutrophil-induced thrombogenic inflammation in SARS-CoV-2 infection.JCI insight · 2025Article
- N-Acetylcysteine in the Treatment of Acute Lung Injury: Perspectives and Limitations.International journal of molecular sciences · 2025Review
- Apoptotic Vesicles Attenuate Acute Lung InjuryInternational journal of nanomedicine · 2025Article
- Role and intervention of PAD4 in NETs in acute respiratory distress syndrome.Respiratory research · 2024Review
- A Narrative Review: The Role of NETs in Acute Respiratory Distress Syndrome/Acute Lung Injury.International journal of molecular sciences · 2024Review
- Article
- Neutrophil autophagy and NETosis in COVID-19: perspectives.Autophagy · 2023Review
- Neutrophil extracellular traps and their implications in airway inflammatory diseases.Frontiers in medicine · 2023Review
- Targeting autophagy regulation in NLRP3 inflammasome-mediated lung inflammation in COVID-19.Clinical immunology (Orlando, Fla.) · 2022Review
- Molecular mechanisms and roles of pyroptosis in acute lung injury.Chinese medical journal · 2022Article
- Redox regulation of the immune response.Cellular & molecular immunology · 2022Review
- Dysregulated miRNAs network in the critical COVID-19: An important clue for uncontrolled immunothrombosis/thromboinflammation.International immunopharmacology · 2022Review
- Recent Developments in the Understanding of Immunity, Pathogenesis and Management of COVID-19.International journal of molecular sciences · 2022Review
- Platelet Dysregulation in the Pathobiology of COVID-19.Hamostaseologie · 2022Review
- Cell deaths: Involvement in the pathogenesis and intervention therapy of COVID-19.Signal transduction and targeted therapy · 2022Review
- Neutrophil extracellular traps in chronic lung disease: implications for pathogenesis and therapy.European respiratory review : an official journal of the European Respiratory Society · 2022Review
- Of vascular defense, hemostasis, cancer, and platelet biology: an evolutionary perspective.Cancer metastasis reviews · 2022Review
- Biomarkers during COVID-19: Mechanisms of Change and Implications for Patient Outcomes.Diagnostics (Basel, Switzerland) · 2022Review
- NLRP3 inflammasome activation in COVID-19: an interlink between risk factors and disease severity.Microbes and infection · 2022Review
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 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCOVID-19-associated acute respiratory distress syndrome (ARDS) is associated with significant morbidity and high levels of mortality. This paper describes the processes involved in the pathophysiology of COVID-19 from the initial infection and subsequent destruction of type II alveolar epithelial cells by SARS-CoV-2 and culminating in the development of ARDS. MAIN BODY: The activation of alveolar cells and alveolar macrophages leads to the release of large quantities of proinflammatory cytokines and chemokines and their translocation into the pulmonary vasculature. The presence of these inflammatory mediators in the vascular compartment leads to the activation of vascular endothelial cells platelets and neutrophils and the subsequent formation of platelet neutrophil complexes. These complexes in concert with activated endothelial cells interact to create a state of immunothrombosis. The consequence of immunothrombosis include hypercoagulation, accelerating inflammation, fibrin deposition, migration of neutrophil extracellular traps (NETs) producing neutrophils into the alveolar apace, activation of the NLRP3 inflammazome, increased alveolar macrophage destruction and massive tissue damage by pyroptosis and necroptosis Therapeutic combinations aimed at ameliorating immunothrombosis and preventing the development of severe COVID-19 are discussed in detail.
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.