title: Protease-activated receptors in cardiovascular health and diseases.
abstract: The platelet, once thought to be solely involved in clot formation, is now known to be a key mediator in various other processes such as inflammation, thrombosis, and atherosclerosis. Therefore, antiplatelet agents have become paramount in the prevention and management of various cardiovascular diseases. However, the currently most widely used antiplatelet drugs, aspirin and clopidogrel, have been shown to reduce the risk of serious vascular events only by approximately one quarter. Similarly, oral glycoprotein IIb/IIIa antagonists have been associated with excess mortality, thus restricting the use of parental glycoprotein IIb/IIIa antagonists to the treatment of acute clinical conditions. Thus, for the prevention of cardiovascular diseases, there is still a clinical need for antiplatelet drugs with higher antithrombotic efficacy but with safety profiles that allow for a preventive long-term administration. Thrombin signaling through the protease-activated receptors (PARs) has been shown to influence a wide range of physiologic and pathologic responses in cardiovascular systems. Thus, interference with PARs appears to be a promising strategy to develop new antiplatelet agents with higher efficacy. This review focuses on the cardiovascular actions of PARs that play a role in normal cardiovascular physiology and that are likely to contribute to cardiovascular diseases.
authors.affiliation: Department of Cardiovascular Medicine, Baylor College of Medicine, Houston, TX, USA. shahcardiology@yahoo.com
authors.forename: Rahman
authors.initials: R
authors.lastname: Shah
mesh_terms: D002318:Cardiovascular Diseases / Q000188:drug therapy*; D002319:Cardiovascular System / Q000187:drug effects; D006801:Humans; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology* / Q000627:therapeutic use; D044462:Receptors, Proteinase-Activated / Q000187:drug effects*
chemical_list: D010975:Platelet Aggregation Inhibitors; D044462:Receptors, Proteinase-Activated