ArticleJournal of thrombosis and haemostasis : JTH2022
Antibody-mediated procoagulant platelet formation in COVID-19 is AKT dependent.
Article in Journal of thrombosis and haemostasis : JTH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Characterizing mouse platelet heterogeneity across diverse disease models using spectral flow cytometry and high-dimensional analysis.Research and practice in thrombosis and haemostasis · 2026Article
- Review
- Platelet-activating histone/antihistone IgG complexes in anti-PF4-negative thrombosis and thrombocytopenia syndrome.Blood advances · 2025Observational
- COVID-19: a vascular nightmare unfolding.Frontiers in immunology · 2025Review
- Complex Pattern of Platelet Activation/Reactivity After SARS-CoV-2 Infection.International journal of molecular sciences · 2024Review
- Genetic signatures ofFrontiers in immunology · 2024Observational
- SARS-CoV-2 Spike Protein and Neutralizing Anti-Spike Protein Antibodies Modulate Blood Platelet Function.International journal of molecular sciences · 2023Article
- Live and let die: signaling AKTivation and UPRegulation dynamics in SARS-CoVs infection and cancer.Cell death & disease · 2022Review
- Procoagulant platelets: novel players in thromboinflammation.American journal of physiology. Cell physiology · 2022Review
- Potential effects of icariin, the Epimedium-derived bioactive compound in the treatment of COVID-19: a hypothesis.Naunyn-Schmiedeberg's archives of pharmacology · 2022Review
- Gene Network Analysis of the Transcriptome Impact of SARS-CoV-2 Interacting MicroRNAs in COVID-19 Disease.International journal of molecular sciences · 2022Review
- Longitudinal multiparametric characterization of platelet dysfunction in COVID-19: Effects of disease severity, anticoagulation therapy and inflammatory status.Thrombosis research · 2022Article
- Platelet-leukocyte interactions in COVID-19: Contributions to hypercoagulability, inflammation, and disease severity.Research and practice in thrombosis and haemostasis · 2022Article
- COVID-19 andJournal of ginseng research · 2022Review
- Platelet Subtypes in Inflammatory Settings.Frontiers in cardiovascular medicine · 2022Review
- Immune-Mediated Platelet Activation in COVID-19 and Vaccine-Induced Immune Thrombotic Thrombocytopenia.Frontiers in immunology · 2022Review
- Platelet in thrombo-inflammation: Unraveling new therapeutic targets.Frontiers in immunology · 2022Review
- Neutrophil-Platelet Interactions as Novel Treatment Targets in Cardiovascular Disease.Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
backgroundThromboembolic events are frequently reported in patients infected with the SARS-CoV-2. Recently, we observed that platelets from patients with severe COVID-19 infection express procoagulant phenotype. The molecular mechanisms that induce the generation of procoagulant platelets in COVID-19 patients are not completely understood.
objectivesIn this study, we investigated the role of AKT (also known as Protein Kinase B), which is the major downstream effector of PI3K (phosphoinositid-3-kinase) (PI3K/AKT) signaling pathway in platelets from patients with COVID-19. PATIENTS AND
methodsPlatelets, Sera and IgG from COVID-19 patients who were admitted to the intensive care unit (ICU) were analyzed by flow cytometry as well as western blot and adhesion assays.
resultsPlatelets from COVID-19 patients showed significantly higher levels of phosphorylated AKT, which was correlated with CD62p expression and phosphatidylserine (PS) externalization. In addition, healthy platelets incubated with sera or IgGs from ICU COVID-19 patients induced phosphorylation of PI3K and AKT and were dependent on Fc-gamma-RIIA (FcγRIIA). In contrast, ICU COVID-19 sera mediated generation of procoagulant platelets was not dependent on GPIIb/IIIa. Interestingly, the inhibition of phosphorylation of both proteins AKT and PI3K prevented the generation of procoagulant platelets.
conclusionsOur study shows that pAKT/AKT signaling pathway is associated with the formation of procoagulant platelets in severe COVID-19 patients without integrin GPIIb/IIIa engagement. The inhibition of PI3K/AKT phosphorylation might represent a promising strategy to reduce the risk for thrombosis in patients with severe COVID-19.
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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.