ReviewLife sciences2020
The pathophysiology of SARS-CoV-2: A suggested model and therapeutic approach.
Review in Life sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 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
65 citing papers in PubMed, 104 citations in OpenAlex.
- Metabolic control of macrophages in coronavirus disease 2019.Virulence · 2026Review
- Cytokine-driven modulation of peripheral immune cell populations in Coronavirus disease 2019 patients.Frontiers in immunology · 2026Article
- The role of programmed cell death in chronic obstructive pulmonary disease: from pathogenesis to treatment.Frontiers in immunology · 2026Review
- Metabolic Reprogramming in Respiratory Viral Infections: A Focus on SARS-CoV-2, Influenza, and Respiratory Syncytial Virus.Biomolecules · 2025Review
- Targeting alveolar macrophages: a promising intervention for pulmonary infection and acute lung injury.Cellular & molecular biology letters · 2025Review
- Dysregulation of neutrophil in sepsis: recent insights and advances.Cell communication and signaling : CCS · 2025Review
- Case report: Causes of acute respiratory distress syndrome complications after lung resection.SAGE open medical case reports · 2025Article
- Resveratrol as a naturally occurring inflammasome modulator: Implications for health and disease.Iranian journal of basic medical sciences · 2025Review
- Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024Review
- Multifaceted role of SARS-CoV-2 structural proteins in lung injury.Frontiers in immunology · 2024Review
- Targeting ferroptosis: a new therapeutic opportunity for kidney diseases.Frontiers in immunology · 2024Review
- Cytokine storm and translating IL-6 biology into effective treatments for COVID-19.Frontiers of medicine · 2023Review
- COVID-19 Complications: Oxidative Stress, Inflammation, and Mitochondrial and Endothelial Dysfunction.International journal of molecular sciences · 2023Review
- SARS-CoV-2 mouse adaptation selects virulence mutations that cause TNF-driven age-dependent severe disease with human correlates.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Structure and Functions of HMGB2 Protein.International journal of molecular sciences · 2023Review
- Convalescent plasma (hyperimmune immunoglobulin) for COVID-19 management: An update.Process biochemistry (Barking, London, England) · 2023Review
- The regulation of lncRNAs and miRNAs in SARS-CoV-2 infection.Frontiers in cell and developmental biology · 2023Review
- Tracking peripheral vascular function for six months in young adults following SARS-CoV-2 infection.Physiological reports · 2022Article
- Redox regulation of the immune response.Cellular & molecular immunology · 2022Review
5 more citing papers are in PubMed but not listed here.
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 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this paper, a model is proposed of the pathophysiological processes of COVID-19 starting from the infection of human type II alveolar epithelial cells (pneumocytes) by SARS-CoV-2 and culminating in the development of ARDS. The innate immune response to infection of type II alveolar epithelial cells leads both to their death by apoptosis and pyroptosis and to alveolar macrophage activation. Activated macrophages secrete proinflammatory cytokines and chemokines and tend to polarise into the inflammatory M1 phenotype. These changes are associated with activation of vascular endothelial cells and thence the recruitment of highly toxic neutrophils and inflammatory activated platelets into the alveolar space. Activated vascular endothelial cells become a source of proinflammatory cytokines and reactive oxygen species (ROS) and contribute to the development of coagulopathy, systemic sepsis, a cytokine storm and ARDS. Pulmonary activated platelets are also an important source of proinflammatory cytokines and ROS, as well as exacerbating pulmonary neutrophil-mediated inflammatory responses and contributing to systemic sepsis by binding to neutrophils to form platelet-neutrophil complexes (PNCs). PNC formation increases neutrophil recruitment, activation priming and extraversion of these immune cells into inflamed pulmonary tissue, thereby contributing to ARDS. Sequestered PNCs cause the development of a procoagulant and proinflammatory environment. The contribution to ARDS of increased extracellular histone levels, circulating mitochondrial DNA, the chromatin protein HMGB1, decreased neutrophil apoptosis, impaired macrophage efferocytosis, the cytokine storm, the toll-like receptor radical cycle, pyroptosis, necroinflammation, lymphopenia and a high Th17 to regulatory T lymphocyte ratio are detailed.
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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.