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

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          Abstract

          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)A 2 is the primary prostanoid that stimulates platelet aggregation; its action is counter‐balanced by prostacyclin, a product of vascular COX. Prostaglandin (PG)D 2, PGE 2 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 P 2Y 12 receptor antagonists for the treatment of cardiovascular diseases is currently debated. Aspirin not only suppresses TXA 2 but also prevents the synthesis of both known and unknown antiplatelet eicosanoid pathways, potentially lessening the efficacy of dual antiplatelet therapies.

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          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

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          Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs.

          J R Vane (1971)
          Article 0 comments Cited 641 times – based on 0 reviews     Review now
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            The effect of celecoxib, a cyclooxygenase-2 inhibitor, in familial adenomatous polyposis.

            G Steinbach, P M Lynch, R K Phillips … (2000)
            Patients with familial adenomatous polyposis have a nearly 100 percent risk of colorectal cancer. In this disease, the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2. We studied the effect of celecoxib, a selective cyclooxygenase-2 inhibitor, on colorectal polyps in patients with familial adenomatous polyposis. In a double-blind, placebo-controlled study, we randomly assigned 77 patients to treatment with celecoxib (100 or 400 mg twice daily) or placebo for six months. Patients underwent endoscopy at the beginning and end of the study. We determined the number and size of polyps from photographs and videotapes; the response to treatment was expressed as the mean percent change from base line. At base line, the mean (+/-SD) number of polyps in focal areas where polyps were counted was 15.5+/-13.4 in the 15 patients assigned to placebo, 11.5+/-8.5 in the 32 patients assigned to 100 mg of celecoxib twice a day, and 12.3+/-8.2 in the 30 patients assigned to 400 mg of celecoxib twice a day (P=0.66 for the comparison among groups). After six months, the patients receiving 400 mg of celecoxib twice a day had a 28.0 percent reduction in the mean number of colorectal polyps (P=0.003 for the comparison with placebo) and a 30.7 percent reduction in the polyp burden (the sum of polyp diameters) (P=0.001), as compared with reductions of 4.5 and 4.9 percent, respectively, in the placebo group. The improvement in the extent of colorectal polyposis in the group receiving 400 mg twice a day was confirmed by a panel of endoscopists who reviewed the videotapes. The reductions in the group receiving 100 mg of celecoxib twice a day were 11.9 percent (P=0.33 for the comparison with placebo) and 14.6 percent (P=0.09), respectively. The incidence of adverse events was similar among the groups. In patients with familial adenomatous polyposis, six months of twice-daily treatment with 400 mg of celecoxib, a cyclooxygenase-2 inhibitor, leads to a significant reduction in the number of colorectal polyps.
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              Low-dose aspirin for the prevention of atherothrombosis.

              Carlo Patrono, Luis A. García Rodríguez, Raffaele Landolfi … (2005)
              Article 0 comments Cited 203 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Timothy D Warner:
                ORCID: http://orcid.org/0000-0003-3988-4408
                t.d.warner@qmul.ac.uk
                Journal
                Journal ID (nlm-ta): Br J Pharmacol
                Journal ID (iso-abbrev): Br. J. Pharmacol
                Journal ID (doi): 10.1111/(ISSN)1476-5381
                Journal ID (publisher-id): BPH
                Title: British Journal of Pharmacology
                Publisher: John Wiley and Sons Inc. (Hoboken )
                ISSN (Print): 0007-1188
                ISSN (Electronic): 1476-5381
                Publication date (Electronic): 19 April 2018
                Publication date (Print): April 2019
                Publication date PMC-release: 19 April 2018
                Volume: 176
                Issue: 8 , Themed Section: Eicosanoids 35 years from the 1982 Nobel: where are we now? Guest Editors: Roderick J Flower and Timothy D Warner ( doiID: 10.1111/bph.v176.8 )
                Pages: 988-999
                Affiliations
                [ 1 ] Centre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry Queen Mary University of London London UK
                Author notes
                [*] [* ] Correspondence Timothy D. Warner, Centre for Immunobiology, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK. E‐mail: t.d.warner@ 123456qmul.ac.uk
                Author information
                http://orcid.org/0000-0003-3164-512X
                http://orcid.org/0000-0001-9120-0734
                http://orcid.org/0000-0003-0904-677X
                http://orcid.org/0000-0003-3988-4408
                Article
                Publisher ID: BPH14196 Other ID: 2017-BJP-1391-RCT-G.R1
                DOI: 10.1111/bph.14196
                PMC ID: 6451075
                PubMed ID: 29512148
                SO-VID: 83f4530f-17f8-414f-812e-93f43f7a9cae
                Copyright © © 2018 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.
                License:

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 08 November 2017
                Date revision received : 21 February 2018
                Date accepted : 22 February 2018
                Page count
                Figures: 4, Tables: 0, Pages: 12, Words: 4772
                Funding
                Funded by: British Heart Foundation
                Award ID: PG/15/47/31591PG/15/79/31777PG/17/40/33028
                Award ID: PG/17/40/33028
                Award ID: PG/15/79/31777
                Award ID: PG/15/47/31591
                Funded by: European Commission
                Award ID: H2020‐MSCA‐ITN‐2015 GA 675111
                Categories
                Subject: Review Article
                Subject: Themed Section: Review Articles
                Custom metadata
                source-schema-version-number 2.0
                component-id bph14196
                cover-date April 2019
                details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_NLMPMC version:5.6.2.1 mode:remove_FC converted:06.04.2019

                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine
                Data availability:
                ScienceOpen disciplines: Pharmacology & Pharmaceutical medicine

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