Laboratory of Biochemistry, Department of Chemistry, University of Ioannina, 45110 Ioannina, Greece.
Curr Vasc Pharmacol. 2012 Sep;10(5):539-49. doi: 10.2174/157016112801784602.
Inflammation of the vascular wall is considered as the principal underlying mechanism in the development of atherosclerosis. Besides their specific functions in haemostasis via thrombus formation after an endothelial injury, a growing body of evidence indicates that platelets play an important role in the inflammatory reactions occurring in the vascular wall as well as in the subsequent tissue repair mechanisms. Platelets interact with activated endothelium as well as with circulating leukocytes and progenitor cells. These interactions, involve direct cell-to-cell interactions as well as autocrine and paracrine pathways, which lead to activation of platelets and their respective cellular counterpart. An increasing body of evidence suggests that antiplatelet therapy may reduce vascular inflammation primarily by inhibiting platelet activation. The aim of the present review is to highlight the molecular basis of platelet-mediated inflammatory response, focusing on the mechanisms underlying the platelet-endothelial cell interaction. The anti-inflammatory effects of current antiplatelet therapies will be also discussed.
血管壁炎症被认为是动脉粥样硬化发展的主要潜在机制。除了在血管内皮损伤后通过血栓形成在止血方面具有特定功能外，越来越多的证据表明，血小板在血管壁发生的炎症反应以及随后的组织修复机制中发挥重要作用。血小板与激活的内皮细胞以及循环白细胞和祖细胞相互作用。这些相互作用涉及直接的细胞间相互作用以及自分泌和旁分泌途径，导致血小板及其各自的细胞对应物的激活。越来越多的证据表明，抗血小板治疗可能通过抑制血小板激活来减轻血管炎症。本综述的目的是强调血小板介导的炎症反应的分子基础，重点关注血小板-内皮细胞相互作用的机制。还将讨论当前抗血小板治疗的抗炎作用。
