Eicosanoids in platelets and the effect of their modulation by aspirin in the cardiovascular system (and beyond)

Platelets are important players in thrombosis and haemostasis with their function being modulated by mediators in the blood and the vascular wall. Among these, eicosanoids can both stimulate and inhibit platelet reactivity. Platelet Cyclooxygenase (COX)‐1‐generated Thromboxane (TX)A2 is the primary...

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Bibliographic Details
Published in:British journal of pharmacology 2019-04, Vol.176 (8), p.988-999
Main Authors: Crescente, Marilena, Menke, Laura, Chan, Melissa V, Armstrong, Paul C, Warner, Timothy D
Format: Article
Language:English
Subjects:
Animals
Antiplatelet therapy
Aspirin
Aspirin - pharmacology
Blood Platelets - drug effects
Blood Platelets - metabolism
Carcinogenesis
Cardiovascular diseases
Cardiovascular system
Cardiovascular System - drug effects
Cardiovascular System - metabolism
Eicosanoids
Eicosanoids - metabolism
Humans
Medical treatment
Platelet aggregation
Platelet Aggregation Inhibitors - pharmacology
Prostacyclin
Prostaglandin E2
Prostaglandin endoperoxide synthase
Review
Themed Section: Review
Thromboembolism
Thrombosis
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Summary:Platelets are important players in thrombosis and haemostasis with their function being modulated by mediators in the blood and the vascular wall. Among these, eicosanoids can both stimulate and inhibit platelet reactivity. Platelet Cyclooxygenase (COX)‐1‐generated Thromboxane (TX)A2 is the primary prostanoid that stimulates platelet aggregation; its action is counter‐balanced by prostacyclin, a product of vascular COX. Prostaglandin (PG)D2, PGE2 and 12‐hydroxyeicosatraenoic acid (HETE), or 15‐HETE, are other prostanoid modulators of platelet activity, but some also play a role in carcinogenesis. Aspirin permanently inhibits platelet COX‐1, underlying its anti‐thrombotic and anti‐cancer action. While the use of aspirin as an anti‐cancer drug is increasingly encouraged, its continued use in addition to P2Y12 receptor antagonists for the treatment of cardiovascular diseases is currently debated. Aspirin not only suppresses TXA2 but also prevents the synthesis of both known and unknown antiplatelet eicosanoid pathways, potentially lessening the efficacy of dual antiplatelet therapies. Linked Articles This article is part of a themed section on Eicosanoids 35 years from the 1982 Nobel: where are we now? To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.8/issuetoc
ISSN:0007-1188
1476-5381
DOI:10.1111/bph.14196