Ząbczyk Michał, Natorska Joanna, Undas Anetta
Department of Thromboembolic Disorders, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland; Krakow Center for Medical Research and Technologies, St. John Paul II Hospital, Kraków, Poland.
Department of Thromboembolic Disorders, Institute of Cardiology, Jagiellonian University Medical College, Kraków, Poland
Pol Arch Intern Med. 2024 Dec 19;134(12). doi: 10.20452/pamw.16884. Epub 2024 Nov 6.
Fibrin formation is pivotal in hemostasis, serving as a temporary barrier to blood loss following vascular injury, while in thrombosis this process is involved in thrombus progression, stability, and recurrence. Growing evidence shows exceptional complexity of processes that determine fibrin clot structure and function, especially lysability, both in health and disease, which might be relevant in the pathogenesis of arterial and venous thromboembolic diseases. In this review, we summarized available data on novel factors that in recent years have been suggested to contribute to prothrombotic fibrin clot properties, involving formation of compact fibrin networks (reduced clot permeability) displaying impaired susceptibility to lysis (prolonged clot lysis time). The factors discussed in this review encompass elevated levels of factor (F)XI, and its activated form (FXIa), protein carbonylation as the most common type of post‑translational modification, neutrophil extracellular traps formation, increased levels of circulating lipopolysaccharide and zonulin, a marker of gut permeability, along with antithrombin deficiency. These factors have been shown to be not only associated with ischemic stroke, myocardial infarction, pulmonary embolism, and cardiovascular death, but also with unfavorably altered fibrin clot characteristics, which underscores clinical relevance of fibrin clot properties. Given preclinical or ongoing studies aimed at modifying some of these factors, in particular FXI/FXIa inhibitors, recent findings might expand our knowledge on fibrin‑related mechanisms of emerging therapeutic agents tested and stimulate further research into new targets for future therapeutic interventions to prevent thromboembolic events.
纤维蛋白形成在止血过程中起关键作用,作为血管损伤后失血的临时屏障,而在血栓形成过程中,这一过程参与血栓的进展、稳定性和复发。越来越多的证据表明,无论是在健康还是疾病状态下,决定纤维蛋白凝块结构和功能,尤其是溶解能力的过程异常复杂,这可能与动脉和静脉血栓栓塞性疾病的发病机制相关。在本综述中,我们总结了近年来提出的有助于形成促血栓性纤维蛋白凝块特性的新因素的现有数据,这些因素涉及致密纤维蛋白网络(降低凝块通透性)的形成,表现出对溶解的敏感性受损(延长凝块溶解时间)。本综述讨论的因素包括因子(F)XI及其活化形式(FXIa)水平升高、作为最常见翻译后修饰类型的蛋白质羰基化、中性粒细胞胞外陷阱形成、循环脂多糖和肠道通透性标志物zonulin水平升高以及抗凝血酶缺乏。这些因素不仅与缺血性中风、心肌梗死、肺栓塞和心血管死亡相关,还与纤维蛋白凝块特征的不利改变相关,这突出了纤维蛋白凝块特性的临床相关性。鉴于旨在改变其中一些因素的临床前或正在进行的研究,特别是FXI/FXIa抑制剂,最近的研究结果可能会扩展我们对正在测试的新兴治疗药物的纤维蛋白相关机制的认识,并刺激对未来预防血栓栓塞事件治疗干预新靶点的进一步研究。