ArticleScientific reports2022
Integrated analysis of transcriptomic data reveals the platelet response in COVID-19 disease.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- SARS-CoV-2 infection promotes lung thrombosis by inducing integrinβ3 expression in vascular endothelial cells.Scientific reports · 2025Article
- Thrombocytopenia in Sepsis.Life (Basel, Switzerland) · 2025Review
- Dengue infection changes the expressions of CD154 and CD148 in human platelets.Virus research · 2025Article
- Deciphering Abnormal Platelet Subpopulations in COVID-19, Sepsis and Systemic Lupus Erythematosus through Machine Learning and Single-Cell Transcriptomics.International journal of molecular sciences · 2024Article
- Alterations in the megakaryocyte transcriptome impacts platelet function in sepsis and COVID-19 infection.Thrombosis research · 2023Article
- Alterations in platelet proteome signature and impaired platelet integrin αJournal of thrombosis and haemostasis : JTH · 2023Article
- The Novel Role of Noncoding RNAs in Modulating Platelet Function: Implications in Activation and Aggregation.International journal of molecular sciences · 2023Review
- Thromboembolic Disease and Cardiac Thrombotic Complication in COVID-19: A Systematic Review.Metabolites · 2022Review
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Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
COVID-19 is associated with an increased risk of thrombotic events. However, the pathogenesis of these complications is unclear and reports on platelet infection and activation by the virus are conflicting. Here, we integrated single-cell transcriptomic data to elucidate whether platelet activation is a specific response to SARS-CoV-2 infection or a consequence of a generalized inflammatory state. Although platelets from patients infected with SARS-CoV-2 over expressed genes involved in activation and aggregation when compared to healthy controls; those differences disappeared when the comparison was made with patients with generalized inflammatory conditions of other etiology than COVID-19. The membrane receptor for the virus, ACE-2, was not expressed by infected or control platelets. Our results suggest that platelet activation in patients with severe COVID-19 is mainly a consequence of a systemic inflammatory state than direct invasion and activation.
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