Blood clot contraction: Mechanisms, pathophysiology, and disease.
Blood clot contraction: Mechanisms, pathophysiology, and disease.
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血凝块收缩：机制，病理生理学和疾病。
DOI：
10.1016/j.rpth.2022.100023
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发表时间：
2023-01
影响因子：
4.6
通讯作者：
Weisel, John W.
中科院分区：
文献类型：
--
作者：
Litvinov, Rustem I.;Weisel, John W.
2022年，在国际血栓与止血学会（ISTH）大会上发表了题为“血块收缩：机制、病理生理学和疾病”的最新讲座。这是对血凝块收缩或回缩的系统描述，由活化的血小板驱动，并导致纤维蛋白网络沿着压缩嵌入的红细胞。凝块收缩的后果包括纤维蛋白-血小板网向凝块外围的重新分布和核心中红细胞的凝聚，随后它们从双凹面形状变形为多面体细胞（多角体细胞）。这些收缩的结构特征已经在来自不同位置的离体血栓中发现，这表明凝块在血管内经历活体内收缩。在止血凝块中，紧密堆积的多角体细胞形成几乎不可渗透的密封，阻止出血并在出血性疾病中受损。在血栓形成中，收缩通过减少血栓阻塞、降低渗透性和改变对纤溶酶的敏感性来促进局部血流。然而，在（促）血栓形成条件下，连续背景血小板活化之后是血小板耗竭、不应性和活体内凝块收缩受损，这与易发生栓塞的较弱血栓相关。因此，检测不完全的体外凝块收缩的测定对于即将发生或正在发生的血栓形成和血栓栓塞具有潜在的诊断和预后价值。总的来说，血凝块和血栓的收缩是一种未被充分认识和研究的过程，其在各种病因的出血和血栓形成中具有致病和临床意义。最后，我们总结了在2022年ISTH大会期间提出的关于这一主题的相关新数据。血小板驱动的血凝块/血栓收缩（回缩）是一种生理机制。收缩引起凝块成分的重新分布和RBC的压缩变形。（前）血栓状态下的收缩由于过度活化的血小板的耗尽而受损。血栓的收缩影响阻塞性、渗透性、纤维蛋白溶解和栓塞性。
A State of the Art lecture titled “Blood Clot Contraction: Mechanisms, Pathophysiology, and Disease” was presented at the International Society on Thrombosis and Haemostasis (ISTH) Congress in 2022. This was a systematic description of blood clot contraction or retraction, driven by activated platelets and causing compaction of the fibrin network along with compression of the embedded erythrocytes. The consequences of clot contraction include redistribution of the fibrin-platelet meshwork toward the periphery of the clot and condensation of erythrocytes in the core, followed by their deformation from the biconcave shape into polyhedral cells (polyhedrocytes). These structural signatures of contraction have been found in ex vivo thrombi derived from various locations, which indicated that clots undergo intravital contraction within the blood vessels. In hemostatic clots, tightly packed polyhedrocytes make a nearly impermeable seal that stems bleeding and is impaired in hemorrhagic disorders. In thrombosis, contraction facilitates the local blood flow by decreasing thrombus obstructiveness, reducing permeability, and changing susceptibility to fibrinolytic enzymes. However, in (pro)thrombotic conditions, continuous background platelet activation is followed by platelet exhaustion, refractoriness, and impaired intravital clot contraction, which is associated with weaker thrombi predisposed to embolization. Therefore, assays that detect imperfect in vitro clot contraction have potential diagnostic and prognostic values for imminent or ongoing thrombosis and thrombotic embolism. Collectively, the contraction of blood clots and thrombi is an underappreciated and understudied process that has a pathogenic and clinical significance in bleeding and thrombosis of various etiologies. Finally, we have summarized relevant new data on this topic presented during the 2022 ISTH Congress. Platelet-driven contraction (retraction) of blood clots/thrombi is a physiologic mechanism. The contraction causes a redistribution of clot components and compressive deformation of RBCs. Contraction in (pro)thrombotic states is impaired due to the exhaustion of hyperactivated platelets. Contraction of thrombi affects obstructiveness, permeability, fibrinolysis, and embologenicity.
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