COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects.
COVID-19 is a systemic vascular hemopathy: insight for mechanistic and clinical aspects.
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DOI：
10.1007/s10456-021-09805-6
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发表时间：
2021-11
期刊：
影响因子：
9.8
通讯作者：
Griffioen AW
中科院分区：
文献类型：
--
作者：
Smadja DM;Mentzer SJ;Fontenay M;Laffan MA;Ackermann M;Helms J;Jonigk D;Chocron R;Pier GB;Gendron N;Pons S;Diehl JL;Margadant C;Guerin C;Huijbers EJM;Philippe A;Chapuis N;Nowak-Sliwinska P;Karagiannidis C;Sanchez O;Kümpers P;Skurnik D;Randi AM;Griffioen AW
由严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）引起的2019冠状病毒病（COVID-19）是一种与血管炎症和内皮损伤相关的全身性疾病。严重形式的SARS-CoV-2感染可诱导急性呼吸窘迫综合征（ARDS），关于COVID-19 ARDS及其灌注缺陷是否与其他原因诱导的ARDS不同，仍存在持续的争论。除了促炎细胞因子（如白细胞介素-1 β [IL-1β]或IL-6）外，由于内皮细胞（EC）功能障碍，还观察到几种主要病理现象：由称为D-二聚体的纤维蛋白降解产物反映的高凝状态、微血栓形成和大血栓形成和病理性血管生成。SARS-CoV-2不太可能直接感染内皮细胞，EC表达ACE-2是一个有争议的问题。事实上，在患有COVID-19的重症患者中报告的内皮损伤更有可能继发于邻近细胞的感染和/或炎症的后果。内皮病可通过不同因子如血管性血友病因子水平的改变引起高凝状态。除了血栓形成事件，病理性血管生成是最近的发现之一。在COVID-19患者的血浆或肺活检中发现了不同促血管生成因子的过度表达，如血管内皮生长因子（VEGF）、碱性成纤维细胞生长因子（FGF-2）或胎盘生长因子（PlGF）。最后，SARS-CoV-2感染诱导与免疫失调和内皮祖细胞动员相关的紧急骨髓生成，导致获得性血液恶性肿瘤或心血管疾病的特征，这在本文中进行了讨论。总之，这篇综述将试图阐明血栓性并发症，病理性血管生成和EC功能障碍的病理生理学，允许更好地了解新的目标和抗血栓协议，以更好地解决血管系统功能障碍。由于治疗SARS-CoV-2感染及其潜在的长期影响涉及靶向血管区室和/或动员未成熟免疫细胞，我们建议将COVID-19及其并发症定义为全身性血管获得性血液病。
Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is presenting as a systemic disease associated with vascular inflammation and endothelial injury. Severe forms of SARS-CoV-2 infection induce acute respiratory distress syndrome (ARDS) and there is still an ongoing debate on whether COVID-19 ARDS and its perfusion defect differs from ARDS induced by other causes. Beside pro-inflammatory cytokines (such as interleukin-1 β [IL-1β] or IL-6), several main pathological phenomena have been seen because of endothelial cell (EC) dysfunction: hypercoagulation reflected by fibrin degradation products called D-dimers, micro- and macrothrombosis and pathological angiogenesis. Direct endothelial infection by SARS-CoV-2 is not likely to occur and ACE-2 expression by EC is a matter of debate. Indeed, endothelial damage reported in severely ill patients with COVID-19 could be more likely secondary to infection of neighboring cells and/or a consequence of inflammation. Endotheliopathy could give rise to hypercoagulation by alteration in the levels of different factors such as von Willebrand factor. Other than thrombotic events, pathological angiogenesis is among the recent findings. Overexpression of different proangiogenic factors such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (FGF-2) or placental growth factors (PlGF) have been found in plasma or lung biopsies of COVID-19 patients. Finally, SARS-CoV-2 infection induces an emergency myelopoiesis associated to deregulated immunity and mobilization of endothelial progenitor cells, leading to features of acquired hematological malignancies or cardiovascular disease, which are discussed in this review. Altogether, this review will try to elucidate the pathophysiology of thrombotic complications, pathological angiogenesis and EC dysfunction, allowing better insight in new targets and antithrombotic protocols to better address vascular system dysfunction. Since treating SARS-CoV-2 infection and its potential long-term effects involves targeting the vascular compartment and/or mobilization of immature immune cells, we propose to define COVID-19 and its complications as a systemic vascular acquired hemopathy.
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