Liver is the largest solid organ in the abdominal cavity, with sinusoid occupying about half of its volume. Under liver disease, hemodynamics in the liver tissue dynamically change, resulting in injury to liver sinusoidal endothelial cells (LSECs). We discuss the injury of LSECs in liver diseases in this article. Generally, in noninflamed tissues, vascular endothelial cells maintain quiescence of circulating leukocytes, and unnecessary blood clotting is inhibited by multiple antithrombotic factors produced by the endothelial cells. In the setting of inflammation, injured endothelial cells lose these functions, defined as inflammatory endotheliopathy. In chronic hepatitis C, inflammatory endotheliopathy in LSECs contributes to platelet accumulation in the liver tissue, and the improvement of thrombocytopenia by splenectomy is attenuated in cases with severe hepatic inflammation. In COVID-19, LSEC endotheliopathy induced by interleukin (IL)-6 trans-signaling promotes neutrophil accumulation and platelet microthrombosis in the liver sinusoids, resulting in liver injury. IL-6 trans-signaling promotes the expression of intercellular adhesion molecule-1, chemokine (C-X-C motif) ligand (CXCL1), and CXCL2, which are the neutrophil chemotactic mediators, and P-selectin, E-selectin, and von Willebrand factor, which are involved in platelet adhesion to endothelial cells, in LSECs. Restoring LSECs function is important for ameliorating liver injury. Prevention of endotheliopathy is a potential therapeutic strategy in liver disease.

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肝脏疾病中肝窦内皮细胞的内皮病变

肝脏是腹腔中最大的实体器官，肝窦约占其体积的一半。在肝脏疾病下，肝组织中的血流动力学发生动态变化，导致肝窦内皮细胞（LSEC）损伤。我们在本文中讨论了肝病中 LSEC 的损伤。一般来说，在非炎症组织中，血管内皮细胞维持循环白细胞的静止，并且内皮细胞产生的多种抗血栓因子抑制不必要的血液凝固。在炎症情况下，受损的内皮细胞失去这些功能，定义为炎症内皮病。在慢性丙型肝炎中，LSEC中的炎性内皮病导致肝组织中的血小板积聚，并且在患有严重肝脏炎症的情况下，脾切除术对血小板减少症的改善作用减弱。在 COVID-19 中，白细胞介素 (IL)-6 反式信号传导诱导的 LSEC 内皮病促进肝窦中中性粒细胞积聚和血小板微血栓形成，导致肝损伤。IL-6 反式信号传导促进细胞间粘附分子 1、趋化因子（CXC 基序）配体 (CXCL1) 和 CXCL2（中性粒细胞趋化介质）以及 P-选择素、E-选择素和冯·维勒布兰德因子的表达，在 LSEC 中，它们参与血小板与内皮细胞的粘附。恢复 LSEC 功能对于改善肝损伤非常重要。预防内皮病是肝病的潜在治疗策略。