University of Utah Molecular Medicine Program in Molecular Medicine, Salt Lake City, Utah.
Division of Microbiology and Pathology, Department of Pathology, University of Utah, Salt Lake City, Utah.
Am J Physiol Cell Physiol. 2022 Oct 1;323(4):C951-C958. doi: 10.1152/ajpcell.00252.2022. Epub 2022 Aug 22.
Platelets play a key role in maintaining hemostasis. However, dysregulated platelet activation can lead to pathological thrombosis or bleeding. Once a platelet gets activated, it will either become an aggregatory platelet or eventually a procoagulant platelet with both types playing distinct roles in thrombosis and hemostasis. Although aggregatory platelets have been extensively studied, procoagulant platelets have only recently come into the spotlight. Procoagulant platelets are a subpopulation of highly activated platelets that express phosphatidylserine and P-selectin on their surface, allowing for coagulation factors to bind and thrombin to be generated. In recent years, novel roles for procoagulant platelets have been identified and they have increasingly been implicated in thromboinflammatory diseases. Here, we provide an up-to-date review on the mechanisms resulting in the formation of procoagulant platelets and how they contribute to hemostasis, thrombosis, and thromboinflammation.
血小板在维持止血中起着关键作用。然而,血小板的异常激活可导致病理性血栓形成或出血。一旦血小板被激活,它将成为聚集性血小板或最终成为促凝性血小板,这两种类型在血栓形成和止血中都起着不同的作用。虽然聚集性血小板已得到广泛研究,但促凝性血小板最近才成为研究热点。促凝性血小板是一种高度激活的血小板亚群,其表面表达磷脂酰丝氨酸和 P 选择素,允许凝血因子结合并生成凝血酶。近年来,促凝性血小板的新作用已被确定,它们越来越多地与血栓炎症性疾病有关。在这里,我们提供了关于导致促凝性血小板形成的机制以及它们如何促进止血、血栓形成和血栓炎症的最新综述。