Department of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, NC, USA.
Curr Opin Hematol. 2018 Sep;25(5):358-364. doi: 10.1097/MOH.0000000000000445.
In spite of significant morbidity and mortality associated with venous thromboembolism, the underlying pathogenesis remains poorly understood.
Clues to operant pathogenic mechanisms are found in the unique morphology and composition of these thrombi, which have substantial red blood cell and fibrin content. Recent studies have revealed biochemical and biophysical mechanisms that dictate fibrin structure in venous thrombi and promote retention of red blood cells within the contracted clots. These mechanisms include newly recognized contributions of fibrin network structure and factor XIII(a)-mediated fibrin crosslinking to venous thrombus composition, size, and stability.
Continued work to elucidate mechanisms by which fibrin(ogen), factor XIII, and red blood cells contribute to venous thrombus formation, structure, and stability may expose novel molecular targets and strategies for reducing thrombosis and thrombotic complications in certain at-risk patients.
尽管静脉血栓栓塞症与显著的发病率和死亡率相关，但发病机制仍知之甚少。
这些血栓独特的形态和组成中存在着作用机制的线索，它们具有大量的红细胞和纤维蛋白含量。最近的研究揭示了决定静脉血栓中纤维蛋白结构并促进红细胞在收缩血栓内保留的生化和生物物理机制。这些机制包括新发现的纤维蛋白网络结构和因子 XIII(a)介导的纤维蛋白交联对静脉血栓组成、大小和稳定性的贡献。
为了阐明纤维蛋白（原）、因子 XIII 和红细胞如何促进静脉血栓形成、结构和稳定性的机制，需要进一步研究，这可能会揭示减少某些高危患者血栓形成和血栓并发症的新的分子靶点和策略。
