Antiplatelet Agents by Jonathan N. Thon Ph.D., Joseph E. Italiano Ph.D. (auth.),

By Jonathan N. Thon Ph.D., Joseph E. Italiano Ph.D. (auth.), Paolo Gresele, Gustav V. R Born, Carlo Patrono, Clive P. Page (eds.)

Antiplatelet remedy is the cornerstone of therapy of ischemic heart problems and during the last few years extraordinary developments during this box were recorded. this is often the 1st finished guide completely devoted to the entire features of antiplatelet treatment. The publication is split into 3 major sections, pathophysiology, pharmacology and remedy, for a complete of 23 chapters. a wide team of major specialists from various eu international locations and from america, either from academia and undefined, have contributed to the booklet. along with a close review at the pharmacology and medical purposes of all of the at the moment used or of the radical antiplatelet brokers, leading edge methods (e.g. intracellular signalling as an antiplatelet objective, small RNAs as platelet therapeutics, etc.) or unconventional features (e.g. pharmacologic modulation of the inflammatory motion of platelets also are taken care of. The booklet is orientated to either simple investigators and to clinicians concerned with study on platelet inhibition or with the scientific use of antiplatelet therapies.

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24 26 27 28 29 29 29 33 37 43 48 50 51 52 Abstract Well-understood functions for “traditional” platelet receptors are described, but “newer” receptors are equally discussed. Receptors are described biochemically (structure, ligand(s), protein partners, and function) and whenever possible, their clinical importance (mutations, polymorphisms, syndrome) are highlighted. Keywords Platelet receptors • Adhesion • Aggregation • Amplification • Stabilization • Thrombosis • Bleeding A. F. be P.

TPa-mediated signal transduction occurs via several G proteins, 40 A. F. Hoylaerts including Gq and G12/13. TP receptors are also expressed in other cell types, relevant to atherothrombosis, such as smooth muscle cells, macrophages, and monocytes (Habib et al. 1999; Hirata et al. 1996). Clinical Importance In several patients, platelet dysfunction has been attributed to an abnormal platelet TXA2 receptor. One mutation (Arg60-Leu) in the first cytoplasmic loop of TPa was found in patients with a mild bleeding disorder, characterized in aggregation tests by altered responses to TXA2, TXA2 analogs, and other agonists (but not thrombin).

2 GPIb-IX-V in Initiation of Platelet Recruitment . . . . . . . . . . . . . . . . . . . . . . 1 Biochemical Description . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2 GPIb, an Omnivalent Receptor . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Bernard–Soulier Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Platelet Adhesion and Aggregation .

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