Department of Laboratory Diagnostics, Pomeranian Medical University, Szczecin, Poland.
J Physiol Pharmacol. 2021 Feb;72(1). doi: 10.26402/jpp.2021.1.01. Epub 2021 Jun 3.
In cardiovascular disease pathogenesis, key roles are played by hypercoagulation disorders mainly associated with platelet activation, aggregation processes, and endothelial dysfunction. Current research is studying new molecular species that might interfere with both previously known and new biochemical pathways, leading to the activation and aggregation of platelets, and growing evidence suggests close links between inflammation and thrombosis. It has been suggested that, in cardiovascular disease, circulating pentameric C-reactive protein (CRP) can dissociate into the monomeric form on activated platelets and the surface of circulating microvesicles, and this could potentially accelerate thrombogenesis and link platelet hemostatic processes with the immune response. Increased microvesicles level has confirmed the link between microvesicles and the inflammatory process in diseases with a strong inflammatory reaction. The treatment of coronary artery disease is partly based on properly selected pharmacotherapy. Despite the significant progress that has recently been made in recognizing and combatting abnormal response to oral antiplatelet agents, it is still unknown why some patients who receive dual antiplatelet therapy do not benefit from expected therapeutic effects. Part of the antithrombotic action that antiplatelet agents exert in different clinical settings may be explained by a modulation in the generation of platelet-derived microvesicles bound monomeric CRP. It is suggested that markers of inflammation, such as monomeric CRP or platelet-derived microvesicles, may provide markers of disease activity or response to treatment and may be used in the prognosis of the course of various diseases. This paper aims to provide an overview of the relationship between the monomeric form of C-reactive protein, associated with membrane microvesicles, higher platelet activation, and the possible association with lower antiplatelet response.
在心血管疾病发病机制中，主要与血小板激活、聚集过程和内皮功能障碍有关的高凝状态起着关键作用。目前的研究正在研究新的分子种类，这些分子可能干扰以前已知和新的生化途径，导致血小板的激活和聚集，越来越多的证据表明炎症和血栓形成之间存在密切联系。有人提出，在心血管疾病中，循环五聚体 C 反应蛋白（CRP）在激活的血小板和循环微泡的表面可以从单体形式解离，这可能潜在地加速血栓形成，并将血小板止血过程与免疫反应联系起来。循环微泡水平的增加证实了微泡与具有强烈炎症反应的疾病中炎症过程之间的联系。冠心病的治疗部分基于适当选择的药物治疗。尽管最近在识别和对抗口服抗血小板药物异常反应方面取得了重大进展，但仍不清楚为什么一些接受双联抗血小板治疗的患者没有从预期的治疗效果中受益。抗血小板药物在不同临床环境中发挥的部分抗血栓作用可能归因于与膜微泡结合的 CRP 单体的血小板衍生微泡生成的调节。有人提出，炎症标志物，如单体 CRP 或血小板衍生的微泡，可能提供疾病活动或对治疗反应的标志物，并可用于各种疾病过程的预后。本文旨在概述 CRP 单体形式、与膜微泡相关的更高血小板激活以及与较低抗血小板反应的可能关联之间的关系。
