COVID-19 Vasculopathy: Mounting Evidence for an Indirect Mechanism of Endothelial Injury.

COVID-19 Vasculopathy: Mounting Evidence for an Indirect Mechanism of Endothelial Injury.
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DOI:
10.1016/j.ajpath.2021.05.007
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发表时间:
2021-08
期刊:
The American journal of pathology
影响因子:
--
通讯作者:
Ribatti D
Ribatti D
中科院分区:
其他
文献类型:
--
作者:
Nicosia RF;Ligresti G;Caporarello N;Akilesh S;Ribatti D

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2019冠状病毒病(COVID-19)重症患者会出现血管并发症,其特征是小、中、大血管血栓形成。严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)感染引起的血管内皮功能障碍与COVID-19血管病变的发病机制有关。虽然最初的报告表明,内皮损伤是由病毒直接引起的,但最近的研究表明,内皮细胞不表达SARS-CoV-2用于进入细胞的受体血管紧张素转换酶2,或以低水平表达,并对感染具有抵抗力。这些新发现,以及COVID-19引发能够损伤内皮并破坏其抗血栓形成特性的细胞因子风暴的观察结果,有利于内皮损伤的间接机制,其通过对受感染的非内皮细胞(如支气管和肺泡上皮)的增强炎症反应局部介导,并通过对感染的过度免疫反应全身介导。在此,我们回顾了COVID-19的血管病理学,并严格讨论了这种疾病中内皮损伤的潜在机制。
Patients with coronavirus disease 2019 (COVID-19) who are critically ill develop vascular complications characterized by thrombosis of small, medium, and large vessels. Dysfunction of the vascular endothelium due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has been implicated in the pathogenesis of the COVID-19 vasculopathy. Although initial reports suggested that endothelial injury was caused directly by the virus, recent studies indicate that endothelial cells do not express angiotensin-converting enzyme 2, the receptor that SARS-CoV-2 uses to gain entry into cells, or express it at low levels and are resistant to the infection. These new findings, together with the observation that COVID-19 triggers a cytokine storm capable of injuring the endothelium and disrupting its antithrombogenic properties, favor an indirect mechanism of endothelial injury mediated locally by an augmented inflammatory reaction to infected nonendothelial cells, such as the bronchial and alveolar epithelium, and systemically by the excessive immune response to infection. Herein we review the vascular pathology of COVID-19 and critically discuss the potential mechanisms of endothelial injury in this disease.
危及生命的Covid-19患者中针对I型IFN的自身抗体。
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