Single-cell RNA analysis on ACE2 expression provides insights into SARS-CoV-2 potential entry into the bloodstream and heart injury
Single-cell RNA analysis on ACE2 expression provides insights into SARS-CoV-2 potential entry into the bloodstream and heart injury
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对 ACE2 表达的单细胞 RNA 分析可深入了解 SARS-CoV-2 进入血液和心脏损伤的可能性
DOI：
10.1002/jcp.29802
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发表时间：
2020-06-08
影响因子：
5.6
通讯作者：
Meng, Dan
中科院分区：
文献类型：
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作者：
Guo, Jieyu;Wei, Xiangxiang;Meng, Dan
2019 冠状病毒病 (COVID-19) 是一种具有高传染性和致病性的全球流行病，已导致全球数万人死亡。最近的研究发现，COVID-19的病原体严重急性呼吸综合征冠状病毒2（SARS-CoV-2）与SARS-CoV具有相同的细胞受体血管紧张素转换酶II（ACE2）。 COVID-19死亡病例的病理学检查显示，肺部具有肺纤维化的特征。然而，SARS-CoV-2如何从肺部传播到其他器官尚未确定。在这里，我们使用已发表的单细胞 RNA-seq 数据，对健康和纤维化肺部以及正常和衰竭成人心脏中 ACE2 的细胞类型特异性表达进行了公正的评估。我们发现纤维化肺中的ACE2表达主要位于动脉血管细胞中，这可能为SARS-CoV-2的血流传播提供了途径。衰竭的人类心脏中表达 ACE2 的心肌细胞比例较高，SARS-CoV-2 可能会通过血流攻击心力衰竭患者的心肌细胞。此外，ACE2在呼吸道合胞病毒或中东呼吸综合征冠状病毒感染的细胞以及脂多糖治疗的小鼠中高表达。我们的研究结果表明，患有肺纤维化、心力衰竭和病毒感染的患者有更高的风险，更容易感染 SARS-CoV-2。 SARS-CoV-2 可能会通过进入血液来攻击其他器官。这项研究为 SARS-CoV-2 血液进入和心脏损伤提供了新的见解，并可能提出一种预防患者出现严重并发症的治疗策略。
Coronavirus disease-2019 (COVID-19) is a global pandemic with high infectivity and pathogenicity, accounting for tens of thousands of deaths worldwide. Recent studies have found that the pathogen of COVID-19, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), shares the same cell receptor angiotensin converting enzyme II (ACE2) as SARS-CoV. The pathological investigation of COVID-19 deaths showed that the lungs had characteristics of pulmonary fibrosis. However, how SARS-CoV-2 spreads from the lungs to other organs has not yet been determined. Here, we performed an unbiased evaluation of cell-type-specific expression of ACE2 in healthy and fibrotic lungs, as well as in normal and failed adult human hearts, using published single-cell RNA-seq data. We found that ACE2 expression in fibrotic lungs mainly locates in arterial vascular cells, which might provide a route for bloodstream spreading of SARS-CoV-2. Failed human hearts have a higher percentage of ACE2-expressing cardiomyocytes, and SARS-CoV-2 might attack cardiomyocytes through the bloodstream in patients with heart failure. Moreover, ACE2 was highly expressed in cells infected by respiratory syncytial virus or Middle East respiratory syndrome coronavirus and in mice treated by lipopolysaccharide. Our findings indicate that patients with pulmonary fibrosis, heart failure, and virus infection have a higher risk and are more susceptible to SARS-CoV-2 infection. The SARS-CoV-2 might attack other organs by getting into the bloodstream. This study provides new insights into SARS-CoV-2 blood entry and heart injury and might propose a therapeutic strategy to prevent patients from developing severe complications.