ArticleDiabetes2012
High glucose inhibits the aspirin-induced activation of the nitric oxide/cGMP/cGMP-dependent protein kinase pathway and does not affect the aspirin-induced inhibition of thromboxane synthesis in human platelets.
Article in Diabetes, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 36 citations in OpenAlex.
- Sweeteners: erythritol, xylitol and cardiovascular risk-friend or foe?Cardiovascular research · 2025Review
- The Interplay between Liver Sinusoidal Endothelial Cells, Platelets, and Neutrophil Extracellular Traps in the Development and Progression of Metabolic Dysfunction-Associated Steatotic Liver Disease.Journal of clinical medicine · 2024Review
- Impact of Physical Exercise on Platelets: Focus on Its Effects in Metabolic Chronic Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- High Levels of Thromboxane (TX) Are Associated with the Sex-Dependent Non-Dipping Phenomenon in Ischemic Stroke Patients.Journal of clinical medicine · 2022Article
- Platelets in Non-alcoholic Fatty Liver Disease.Frontiers in pharmacology · 2022Review
- The Role of Thromboxane in the Course and Treatment of Ischemic Stroke: Review.International journal of molecular sciences · 2021Review
- Effect of prediabetes on asprin or clopidogrel resistance in patients with recent ischemic stroke/TIA.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- Association between High On-Aspirin Platelet Reactivity and Reduced Superoxide Dismutase Activity in Patients Affected by Type 2 Diabetes Mellitus or Primary Hypercholesterolemia.International journal of molecular sciences · 2020Article
- Influence of Cardiometabolic Risk Factors on Platelet Function.International journal of molecular sciences · 2020Review
- Glucagon-like peptide 1-related peptides increase nitric oxide effects to reduce platelet activation.Thrombosis and haemostasis · 2017Article
- Platelets, diabetes and myocardial ischemia/reperfusion injury.Cardiovascular diabetology · 2017Review
- Younger age, higher body mass index and lower adiponectin concentration predict higher serum thromboxane B2 level in aspirin-treated patients with type 2 diabetes: an observational study.Cardiovascular diabetology · 2014Observational
- Involvement of RhoA/ROCK1 signaling pathway in hyperglycemia-induced microvascular endothelial dysfunction in diabetic retinopathy.International journal of clinical and experimental pathology · 2014Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Since hyperglycemia is involved in the "aspirin resistance" occurring in diabetes, we aimed at evaluating whether high glucose interferes with the aspirin-induced inhibition of thromboxane synthesis and/or activation of the nitric oxide (NO)/cGMP/cGMP-dependent protein kinase (PKG) pathway in platelets. For this purpose, in platelets from 60 healthy volunteers incubated for 60 min with 5-25 mmol/L d-glucose or iso-osmolar mannitol, we evaluated the influence of a 30-min incubation with lysine acetylsalicylate (L-ASA; 1-300 μmol/L) on 1) platelet function under shear stress; 2) aggregation induced by sodium arachidonate or ADP; 3) agonist-induced thromboxane production; and 4) NO production, cGMP synthesis, and PKG-induced vasodilator-stimulated phosphoprotein phosphorylation. Experiments were repeated in the presence of the antioxidant agent amifostine. We observed that platelet exposure to 25 mmol/L d-glucose, but not to iso-osmolar mannitol, 1) reduced the ability of L-ASA to inhibit platelet responses to agonists; 2) did not modify the L-ASA-induced inhibition of thromboxane synthesis; and 3) prevented the L-ASA-induced activation of the NO/cGMP/PKG pathway. Preincubation with amifostine reversed the high-glucose effects. Thus, high glucose acutely reduces the antiaggregating effect of aspirin, does not modify the aspirin-induced inhibition of thromboxane synthesis, and inhibits the aspirin-induced activation of the NO/cGMP/PKG pathway. These results identify a mechanism by which high glucose interferes with the aspirin action.
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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.