ArticleJournal of cellular and molecular medicine2020
The microvesicle/CD36 complex triggers a prothrombotic phenotype in patients with non-valvular atrial fibrillation.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Role of NADPH oxidase 2-derived reactive oxygen species in cardiac electrophysiological disorders.Channels (Austin, Tex.) · 2026Review
- Levels of Talin1 in Platelet-Derived Microvesicles Affect Platelet Activation in Patients with Nonvalvular Atrial Fibrillation.Biochemical genetics · 2026Article
- Extracellular Vesicles in Atrial Fibrillation-State of the Art.International journal of molecular sciences · 2022Review
- Extracellular Vesicles and Thrombogenicity in Atrial Fibrillation.International journal of molecular sciences · 2022Review
- Platelet CD36 links overweight and a prothrombotic phenotype in patients with non-valvular atrial fibrillation.Frontiers in cardiovascular medicine · 2022Article
- The microvesicle/CD36 complex triggers a prothrombotic phenotype in patients with non-valvular atrial fibrillation.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanisms responsible for platelet activation, the prothrombotic state, in non-valvular atrial fibrillation (NVAF) are still obscure. Microvesicles (MVs) can transfer various messages to target cells and may be helpful for exploring the detailed mechanisms. We aimed to investigate the possible mechanisms by which proatherogenic factors of NVAF contribute to platelet activation. Two hundred and ten patients with NVAF were stratified as being at 'low to moderate risk' or 'high risk' for stroke according to the CHADS2 score. Levels of platelet-derived MVs (PMVs) and platelet activation were examined. CD36-positive or CD36-deficient human platelets were stimulated by MVs isolated from NVAF patients with or without various inhibitors in vitro. Levels of PMVs and platelet activation markers enhanced significantly in high-risk patients. The MVs isolated from plasma of NVAF patients bound to platelet CD36 and activated platelets by phosphorylating the mitogen-activated protein kinase 4/Jun N-terminal kinase 2 (MKK4/JNK2) pathways. However, CD36 deficiency protected against MV-induced activation of platelets. We reveal a possible mechanism of platelet activation in NVAF and suggest that the platelet CD36 might be an effective target in preventing the prothrombotic state in NVAF.
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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.