ArticleJournal of hematology & oncology2020
SARS-CoV-2 binds platelet ACE2 to enhance thrombosis in COVID-19.
Article in Journal of hematology & oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 405 papers, 2 of them syntheses 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
405 citing papers in PubMed, 2 syntheses or guidelines pooled it, 678 citations in OpenAlex.
- Risk of thromboembolism in patients with COVID-19 who are using hormonal contraception: a Cochrane systematic review.BMJ sexual & reproductive health · 2023Pooled it
- Risk of thromboembolism in patients with COVID-19 who are using hormonal contraception.The Cochrane database of systematic reviews · 2023Pooled it
- Platelet-to-Lymphocyte Ratio-A Real or Fake Bridge Between Inflammation and Coagulation in COVID-19 Patients: A Scoping Review.Diagnostics (Basel, Switzerland) · 2026Review
- Antiplatelet activity of a Korean red ginseng-derived saponin fraction and its inhibition of influenza A virus-induced thrombosis.Journal of ginseng research · 2026Article
- Current status and future perspectives on the mechanistic and pathophysiological understanding of long COVID.Communications medicine · 2026Article
- SARS-CoV-2 Omicron variant spike protein maintains the ability to bind and activate human platelets: Comparison with the wild-type.Scientific reports · 2026Article
- Article
- Review
- Increased metallopeptidase activity, compromised endothelial integrity and impaired pathogen recognition revealed by transcriptomics inCurrent research in parasitology & vector-borne diseases · 2026Article
- Association of neutrophil-to-lymphocyte-platelet ratio with residual renal function in early-stage peritoneal dialysis patients.Frontiers in nephrology · 2026Article
- A Boolean Seven-Layer Platelet Decision Model Models Consistently the Logic and Semiquantitatively the Dynamics of Platelet Activation and Inhibition.Computational and structural biotechnology journal · 2026Article
- Comparative systemic pathogenicity and host tropism of ancestral SARS-CoV-2, Delta, and Omicron EG.5 variants in K18-hACE2 mice.Frontiers in immunology · 2026Article
- Megakaryocyte phenotyping in response to SARS-CoV-2 variants.Platelets · 2025Article
- Toxicity study of SARS-CoV-2 Spike protein expressed on Bacillus subtilis spores.BMC microbiology · 2025Article
- Spatial Transcriptomics and Single Cell-RNASeq Reveals Cellular Heterogeneity of SARS-CoV-2 in Lung Tissues and Global Mutational Patterns in COVID-19 Patients.Journal of medical virology · 2025Article
- Integrated microfluidic platforms for extracellular vesicles: Separation, detection, and clinical translation.APL bioengineering · 2025Review
- Alterations in the Platelet Transcriptome Mediate Prenatal Thirdhand Smoke Exposure Associated Thrombogenicity via Integrated miRNA-mRNA Regulatory Networks.International journal of molecular sciences · 2025Article
- Afucosylated IgG Promote Thrombosis in Mouse Injected with SARS-CoV-2 Spike Expressing Megakaryocytes.International journal of molecular sciences · 2025Article
- Vascular Pathogenesis in Acute and Long COVID: Current Insights and Therapeutic Outlook.Seminars in thrombosis and hemostasis · 2025Review
- Chest computed tomography and plain radiographs demonstrate vascular distribution and characteristics in COVID-19 lung disease - a pulmonary vasculopathy.The Ulster medical journal · 2025Article
345 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
17 authors at 5 institutions in 2 countries.
Funding
Abstract
backgroundCritically ill patients diagnosed with COVID-19 may develop a pro-thrombotic state that places them at a dramatically increased lethal risk. Although platelet activation is critical for thrombosis and is responsible for the thrombotic events and cardiovascular complications, the role of platelets in the pathogenesis of COVID-19 remains unclear.
methodsUsing platelets from healthy volunteers, non-COVID-19 and COVID-19 patients, as well as wild-type and hACE2 transgenic mice, we evaluated the changes in platelet and coagulation parameters in COVID-19 patients. We investigated ACE2 expression and direct effect of SARS-CoV-2 virus on platelets by RT-PCR, flow cytometry, Western blot, immunofluorescence, and platelet functional studies in vitro, FeCl
resultsWe demonstrated that COVID-19 patients present with increased mean platelet volume (MPV) and platelet hyperactivity, which correlated with a decrease in overall platelet count. Detectable SARS-CoV-2 RNA in the blood stream was associated with platelet hyperactivity in critically ill patients. Platelets expressed ACE2, a host cell receptor for SARS-CoV-2, and TMPRSS2, a serine protease for Spike protein priming. SARS-CoV-2 and its Spike protein directly enhanced platelet activation such as platelet aggregation, PAC-1 binding, CD62P expression, α granule secretion, dense granule release, platelet spreading, and clot retraction in vitro, and thereby Spike protein enhanced thrombosis formation in wild-type mice transfused with hACE2 transgenic platelets, but this was not observed in animals transfused with wild-type platelets in vivo. Further, we provided evidence suggesting that the MAPK pathway, downstream of ACE2, mediates the potentiating role of SARS-CoV-2 on platelet activation, and that platelet ACE2 expression decreases following SARS-COV-2 stimulation. SARS-CoV-2 and its Spike protein directly stimulated platelets to facilitate the release of coagulation factors, the secretion of inflammatory factors, and the formation of leukocyte-platelet aggregates. Recombinant human ACE2 protein and anti-Spike monoclonal antibody could inhibit SARS-CoV-2 Spike protein-induced platelet activation.
conclusionsOur findings uncovered a novel function of SARS-CoV-2 on platelet activation via binding of Spike to ACE2. SARS-CoV-2-induced platelet activation may participate in thrombus formation and inflammatory responses in COVID-19 patients.
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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.