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. 2018 Feb 14;114(5):645–655. doi: 10.1093/cvr/cvy044

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© The Author(s) 2018. Published by Oxford University Press on behalf of the European Society of Cardiology.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Inhibition of platelet function by RAR and RXR ligands is mediated through Arp2/3- and Gq-induced Rac activation and up-regulation of PKA activity, respectively. RAR ligand atRA disrupts the RARα–Arp2/3 interaction resulting in an inhibition of cytoskeletal rearrangements and platelet spreading. RXR ligands, 9cRA and methoprene acid inhibit platelet activation to a range of platelet agonists that include GPCR agonists (ADP, U46619 or thrombin) and GPVI agonists (collagen or CRP-XL). Interaction of RXR with Gq and subsequent negative regulation of Rac activation is one of the probable explanations for the reduction in GPCR-mediated platelet activation. These ligands have also been shown to up-regulate PKA activity in a cAMP- and NFκβ-dependent manner providing a more generalized mechanism of inhibition.