ArticleBlood advances2022
Upregulation of cAMP prevents antibody-mediated thrombus formation in COVID-19.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- A Systematic Review of the Role of Purinergic Signalling Pathway in the Treatment of COVID-19.International journal of molecular sciences · 2023Pooled it
- Monovalent Anti-FcγRIIA Antibody Blocks Immune-Mediated Thrombocytopenia and Thrombosis With Minimal Adverse Side Effects in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Genes Encoding Heat Shock Proteins Are Associated with Risk and Clinical Course of Severe COVID-19: A Pilot Study.International journal of molecular sciences · 2025Article
- Platelet spleen tyrosine kinase is a key regulator of anti-PF4 antibody-induced immunothrombosis.Blood advances · 2025Article
- Complex Pattern of Platelet Activation/Reactivity After SARS-CoV-2 Infection.International journal of molecular sciences · 2024Review
- Article
- Platelet phosphatidylserine is the critical mediator of thrombosis in heparin-induced thrombocytopenia.Haematologica · 2023Article
- Common molecular signatures between coronavirus infection and Alzheimer's disease reveal targets for drug development.bioRxiv : the preprint server for biology · 2023Article
- SARS-CoV-2 Spike Protein and Neutralizing Anti-Spike Protein Antibodies Modulate Blood Platelet Function.International journal of molecular sciences · 2023Article
- Platelet-neutrophil interaction in COVID-19 and vaccine-induced thrombotic thrombocytopenia.Frontiers in immunology · 2023Review
- Common Molecular Signatures Between Coronavirus Infection and Alzheimer's Disease Reveal Targets for Drug Development.Journal of Alzheimer's disease : JAD · 2023Article
- Procoagulant platelets: novel players in thromboinflammation.American journal of physiology. Cell physiology · 2022Review
- Antibody-mediated procoagulant platelet formation in COVID-19 is AKT dependent.Journal of thrombosis and haemostasis : JTH · 2022Article
- Editorial: Platelet Function in COVID-19.Frontiers in cardiovascular medicine · 2022Article
- 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
- Association of hyperglycaemia with hospital mortality in nondiabetic COVID-19 patients: A cohort study.Diabetes & metabolism · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Thromboembolic events are frequently reported in patients infected with the SARS-CoV-2 virus. The exact mechanisms of COVID-19-associated hypercoagulopathy, however, remain elusive. Recently, we observed that platelets (PLTs) from patients with severe COVID-19 infection express high levels of procoagulant markers, which were found to be associated with increased risk for thrombosis. In the current study, we investigated the time course as well as the mechanisms leading to procoagulant PLTs in COVID-19. Our study demonstrates the presence of PLT-reactive IgG antibodies that induce marked changes in PLTs in terms of increased inner-mitochondrial transmembrane potential (Δψ) depolarization, phosphatidylserine (PS) externalization, and P-selectin expression. The IgG-induced procoagulant PLTs and increased thrombus formation were mediated by ligation of PLT Fc-γ RIIA (FcγRIIA). In addition, contents of calcium and cyclic-adenosine-monophosphate (cAMP) in PLTs were identified to play a central role in antibody-induced procoagulant PLT formation. Most importantly, antibody-induced procoagulant events, as well as increased thrombus formation in severe COVID-19, were inhibited by Iloprost, a clinically approved therapeutic agent that increases the intracellular cAMP levels in PLTs. Our data indicate that upregulation of cAMP could be a potential therapeutic target to prevent antibody-mediated coagulopathy in COVID-19 disease.
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.