INSERM, U1059, SAINBIOSE, Jean Monnet University, F-42023 Saint-Etienne, France.
French Blood Establishment (EFS) Auvergne Rhône Alpes-Scientific Department, F-42270 Saint-Etienne, France.
Int J Mol Sci. 2022 Oct 29;23(21):13176. doi: 10.3390/ijms232113176.
Venous thromboembolism (VTE) is the third leading cardiovascular cause of death and is conventionally treated with anticoagulants that directly antagonize coagulation. However, recent data have demonstrated that also platelets play a crucial role in VTE pathophysiology. In the current review, we outline how platelets are involved during all stages of experimental venous thrombosis. Platelets mediate initiation of the disease by attaching to the vessel wall upon which they mediate leukocyte recruitment. This process is referred to as immunothrombosis, and within this novel concept inflammatory cells such as leukocytes and platelets directly drive the progression of VTE. In addition to their involvement in immunothrombosis, activated platelets can directly drive venous thrombosis by supporting coagulation and secreting procoagulant factors. Furthermore, fibrinolysis and vessel resolution are (partly) mediated by platelets. Finally, we summarize how conventional antiplatelet therapy can prevent experimental venous thrombosis and impacts (recurrent) VTE in humans.
静脉血栓栓塞症（VTE）是心血管疾病导致死亡的第三大原因，传统上采用直接拮抗凝血的抗凝剂进行治疗。然而，最近的数据表明，血小板在 VTE 病理生理学中也起着至关重要的作用。在本次综述中，我们概述了血小板在实验性静脉血栓形成的所有阶段是如何参与的。血小板通过附着在血管壁上而介导白细胞募集，从而启动疾病。这个过程被称为免疫血栓形成，在这个新概念中，白细胞和血小板等炎症细胞直接驱动 VTE 的进展。除了参与免疫血栓形成外，激活的血小板还可以通过支持凝血和分泌促凝因子直接驱动静脉血栓形成。此外，纤维蛋白溶解和血管消退（部分）由血小板介导。最后，我们总结了常规抗血小板治疗如何预防实验性静脉血栓形成以及对人类（复发性）VTE 的影响。
