Adenosine is an important mediator of inhibition of platelet activation. This metabolite is released from various cells, as well as generated via activity of ecto-enzymes on the cell surface. Binding of adenosine to A(2) subtypes (A(2A) or A(2B)), G-protein coupled adenosine receptors, results in increased levels of intracellular cyclic adenosine monophosphate (cAMP), a strong inhibitor of platelet activation. The role and importance of adenosine and its receptors in platelet physiology are addressed in this review, including recently identified roles for the A(2B) adenosine receptor as a modulator of platelet activation through its newly described role in the control of expression of adenosine diphosphate (ADP) receptors.
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http://dx.doi.org/10.1002/jcp.22379 | DOI Listing |
Redox Biol
January 2025
School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China; Key Laboratory of Medical Electrophysiology, Ministry of Education & Medical Electrophysiological Key Laboratory of Sichuan Province, (Collaborative Innovation Center for Prevention of Cardiovascular Diseases), Institute of Cardiovascular Research, Southwest Medical University, Luzhou, 646000, China. Electronic address:
Platelets, which are vital for blood clotting and immunity, need to maintain a delicately balanced relationship between generation and destruction. Recent studies have highlighted that reactive oxygen species (ROS), which act as second messengers in crucial signaling pathways, are crucial players in this dance. This review explores the intricate connection between ROS and platelets, highlighting their dual nature.
View Article and Find Full Text PDFFront Pharmacol
December 2024
Systems Pharmacology and Translational Therapeutics Laboratory, The Center for Advanced Studies and Technology (CAST), "G. d'Annunzio" University, Chieti, Italy.
Inflammation plays a critical role in the pathogenesis of various diseases by promoting the acquisition of new functional traits by different cell types. Shared risk factors between cardiovascular disease and cancer, including smoking, obesity, diabetes, high-fat diet, low physical activity, and alcohol consumption, contribute to inflammation linked to platelet activation. Platelets contribute to an inflammatory state by activating various normal cells, such as fibroblasts, immune cells, and vascular cells.
View Article and Find Full Text PDFDrugs Context
December 2024
2nd Department of Cardiology, National and Kapodistrian University of Athens, Athens, Greece.
Lipoprotein(a) [Lp(a)] is a well-established cardiovascular disease (CVD) risk factor with elevated Lp(a) levels contributing to a higher incidence of atherosclerotic CVD (ASCVD). However, no Lp(a)-specific interventions are currently available in the primary CVD prevention in individuals with elevated Lp(a) levels. RNA-based therapies targeting Lp(a) are under investigation in phase III clinical trials.
View Article and Find Full Text PDFBackground: Germline haplodeficiency (RHD) is associated with thrombocytopenia, platelet dysfunction and predisposition to myeloid malignancies. Platelet expression profiling of a RHD patient showed decreased encoding for the A subunit of factor XIII, a transglutaminase that cross-links fibrin and induces clot stabilization. FXIII-A is synthesized by hematopoietic cells, megakaryocytes and monocytes.
View Article and Find Full Text PDFHIV Res Clin Pract
December 2025
National Heart and Lung Institute, Imperial College London, London, UK.
Introduction: The BIC-T&T study aimed to determine the efficacy of bictegraviremtricitabine/tenofovir alafenamide (BIC/F/TAF) and darunavir/cobicistat/emtricitabinetenofovir alafenamide (DRV/c/F/TAF) at suppressing viral load in a two-arm, open-label, multi-centre, randomised trial under a UK test-and-treat setting. This sub-study aimed to evaluate potential off-target cardiovascular impact by examining platelet function.
Methods: Platelets were isolated by centrifugation of citrated blood from participants attending Chelsea and Westminster Hospital or St Mary's Hospital at Week 48 following enrolment.
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