Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is causing the current coronavirus disease (COVID-19) pandemic [1]. Over recent months, a plethora of novel research articles has been published, dealing with multiple aspects and manifestations of the disease. Increasing evidence points to a central role of endothelial cells in SARS-CoV-2 infection [2–5]. Early studies have already indicated increased expression of vascular and inflammatory factors (such as vascular cell adhesion molecule (VCAM)-1, interleukin (IL)-8 or monocyte-chemoattractant protein (MCP)-1) in COVID-19 lung tissue [2]. Such markers of endothelial dysfunction and altered endothelial cell integrity are important predictors of a poor outcome in SARS-CoV-2 infections [6], and they are associated with pulmonary oedema, intravascular thrombosis and acute respiratory distress syndrome (ARDS). The pulmonary endothelium is crucial for regulation of vascular tone, inflammatory responses, coagulation/fibrinolysis and maintenance of vascular homeostasis and permeability. Disturbances of these tightly regulated processes may directly contribute to morbidity and mortality. However, the exact mechanisms leading to pulmonary vasculopathy in COVID-19 are still unclear. Here, we provide an analysis of several important vascular markers implicated in the inflammatory response (E-selectin, intercellular cell adhesion molecule (ICAM)-1, VCAM-1), maintenance of microvascular integrity (CD31, vascular endothelial growth factor receptor (VEGFR)-2), platelet activation and coagulation (P-selectin, von Willebrand factor (vWF)) in lung tissue and plasma samples of COVID-19 patients.

严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 正在引起当前的冠状病毒病 (COVID-19) 大流行 [1]。最近几个月，发表了大量新颖的研究文章，涉及该疾病的多个方面和表现。越来越多的证据表明内皮细胞在 SARS-CoV-2 感染中的核心作用 [2-5]。早期研究已经表明，COVID-19 肺组织中血管和炎症因子（例如血管细胞粘附分子 (VCAM)-1、白细胞介素 (IL)-8 或单核细胞趋化蛋白 (MCP)-1）的表达增加 [2] ]。这些内皮功能障碍和内皮细胞完整性改变的标志物是 SARS-CoV-2 感染结果不佳的重要预测因素 [6]，并且它们与肺水肿有关，血管内血栓形成和急性呼吸窘迫综合征 (ARDS)。肺内皮对于调节血管张力、炎症反应、凝血/纤溶以及维持血管稳态和通透性至关重要。这些受到严格监管的过程的干扰可能直接导致发病率和死亡率。然而，导致 COVID-19 肺血管病变的确切机制仍不清楚。在这里，我们分析了几个与炎症反应有关的重要血管标志物（E-选择素、细胞间细胞粘附分子 (ICAM)-1、VCAM-1）、微血管完整性的维持（CD31、血管内皮生长因子受体（VEGFR） )-2)、COVID-19 患者肺组织和血浆样本中的血小板活化和凝血（P-选择素、血管性血友病因子 (vWF)）。