Siegel-Axel Dorothea, Langer Harald, Lindemann Stephan, Gawaz Meinrad
Abteilung Kardiologie und Kreislauferkrankungen, Medizinische Klinik III, Eberhard-Karls-Universität, Tübingen.
Med Klin (Munich). 2006 Jun 15;101(6):467-75. doi: 10.1007/s00063-006-1066-0.
Platelets are an important link between inflammation, thrombosis, and atherogenesis. Inflammation is characterized by interactions among platelets, leukocytes, and endothelial cells. These interactions trigger autocrine and paracrine activation processes that lead to leukocyte recruitment into the vascular wall. Platelet-induced chronic inflammatory processes at the vascular wall result in development of atherosclerotic lesions and atherothrombosis.
In vitro studies with co-incubated human endothelial cells and platelets after physical denudation or activation of the endothelium by cytokines provided important results for the understanding of adhesion mechanisms and the involvement of different adhesion receptors, like integrins and selectins. Furthermore, in in vivo mouse models platelet-endothelium interactions under dynamic flow conditions and increased shear stress could be analyzed. With the help of intravital microscopy, the availability of appropriate atherosclerotic animal models and first conclusive data obtained in humans, the important role of platelets in atheroprogression could be confirmed in vivo.
This review highlights the molecular machinery and inflammatory pathways used by platelets to initiate and accelerate atherothrombosis. Understanding the specific requirements for platelets adhering to endothelium may lead to the development of novel therapeutic strategies.
血小板是炎症、血栓形成和动脉粥样硬化发生之间的重要联系环节。炎症的特征是血小板、白细胞和内皮细胞之间的相互作用。这些相互作用触发自分泌和旁分泌激活过程，导致白细胞募集到血管壁。血小板在血管壁诱导的慢性炎症过程导致动脉粥样硬化病变和动脉粥样硬化血栓形成。
通过体外研究，在物理剥脱或细胞因子激活内皮后将人内皮细胞与血小板共同孵育，为理解黏附机制以及不同黏附受体（如整合素和选择素）的参与提供了重要结果。此外，在体内小鼠模型中，可以分析动态流动条件下和剪切应力增加时的血小板 - 内皮细胞相互作用。借助活体显微镜检查、合适的动脉粥样硬化动物模型以及在人类中获得的首批确凿数据，可以在体内证实血小板在动脉粥样硬化进展中的重要作用。
本综述强调了血小板用于启动和加速动脉粥样硬化血栓形成的分子机制和炎症途径。了解血小板黏附于内皮的特定要求可能会导致开发新的治疗策略。
