ArticleBlood advances2018
Platelet CD36 signaling through ERK5 promotes caspase-dependent procoagulant activity and fibrin deposition in vivo.
Article in Blood advances, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed.
- Metrnl Reduces Thrombosis and Acute Myocardial Injury Through Inhibition of Platelet Activation via CD36 Receptor Degradation.Circulation · 2026Article
- Inherited Platelet GPIV Deficiency: First Description of a Series of Unrelated Patients with Bleeding Diathesis.Biomolecules · 2026Article
- Platelet homeostasis and heterogeneity in inflammation and sepsis: mechanisms, biological effects, and clinical potential.Cell communication and signaling : CCS · 2026Review
- CD36 as a Context-Dependent Regulator of Metabolic Switching in Acute and Chronic Hypoxia.Biomolecules · 2026Review
- Procoagulant platelets: linking coagulation and thromboinflammation in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- The Fatty Acid Transporter CD36 Mediates Uptake, Biodistribution, and Cardioprotection by Small Extracellular Vesicles From HEK293 Cells.Journal of extracellular vesicles · 2026Article
- The immune receptor FcRγ-chain mediates CD36-induced platelet activation and thrombosis by oxidized low-density lipoproteins.Blood advances · 2025Article
- NADPH oxidase 2 inhibitor GSK2795039 exerts antiplatelet and antithrombotic activity.Scientific reports · 2025Article
- Mechanical Biomimetic Nanocomposites for Multidimensional Treatment of Arterial Thrombosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Antiplatelet Effects of DMPC-Based Synthetic High-Density Lipoproteins: Exploring Particle Structure and Noncholesterol Efflux Mechanisms.Molecular pharmaceutics · 2025Article
- Sulforaphane attenuates aldose reductase-mediated platelet dysfunction in high glucose-stimulated human platelets via downregulation of the Src/ROS/p53 signaling pathway.Frontiers in nutrition · 2025Article
- Targeting Cysteine Oxidation in Thrombotic Disorders.Antioxidants (Basel, Switzerland) · 2024Review
- OxLDL/LOX-1 mediated sex, age, stiffness, and endothelial dependent alterations in mouse thoracic aortic vascular reactivity.Frontiers in physiology · 2024Article
- Cysteine and methionine oxidation in thrombotic disorders.Current opinion in chemical biology · 2023Review
- Prognostic Value of the Selected Polymorphisms in theBiomedicines · 2023Article
- Effect of antiplatelet agents and tyrosine kinase inhibitors on oxLDL-mediated procoagulant platelet activity.Blood advances · 2023Article
- The significance of ERK5 catalytic-independent functions in disease pathways.Frontiers in cell and developmental biology · 2023Review
- Targeting macrophages in atherosclerosis using nanocarriers loaded with liver X receptor agonists: A narrow review.Frontiers in molecular biosciences · 2023Review
- Procoagulant platelets: novel players in thromboinflammation.American journal of physiology. Cell physiology · 2022Review
- Platelet Redox Imbalance in Hypercholesterolemia: A Big Problem for a Small Cell.International journal of molecular sciences · 2022Review
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Dyslipidemia is a risk factor for clinically significant thrombotic events. In this condition, scavenger receptor CD36 potentiates platelet reactivity through recognition of circulating oxidized lipids. CD36 promotes thrombosis by activating redox-sensitive signaling molecules, such as the MAPK extracellular signal-regulated kinase 5 (ERK5). However, the events downstream of platelet ERK5 are not clear. In this study, we report that oxidized low-density lipoprotein (oxLDL) promotes exposure of procoagulant phosphatidylserine (PSer) on platelet surfaces. Studies using pharmacologic inhibitors indicate that oxLDL-CD36 interaction-induced PSer exposure requires apoptotic caspases in addition to the downstream CD36-signaling molecules Src kinases, hydrogen peroxide, and ERK5. Caspases promote PSer exposure and, subsequently, recruitment of the prothrombinase complex, resulting in the generation of fibrin from the activation of thrombin. Caspase activity was observed when platelets were stimulated with oxLDL. This was prevented by inhibiting CD36 and ERK5. Furthermore, oxLDL potentiates convulxin/glycoprotein VI-mediated fibrin formation by platelets, which was prevented when CD36, ERK5, and caspases were inhibited. Using 2 in vivo arterial thrombosis models in apoE-null hyperlipidemic mice demonstrated enhanced arterial fibrin accumulation upon vessel injury. Importantly, absence of ERK5 in platelets or mice lacking CD36 displayed decreased fibrin accumulation in high-fat diet-fed conditions comparable to that seen in chow diet-fed animals. These findings suggest that platelet signaling through CD36 and ERK5 induces a procoagulant phenotype in the hyperlipidemic environment by enhancing caspase-mediated PSer exposure.
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