ty -jour t1-内皮到间充质转变：旋转后19间间质肺纤维化和血管闭塞的先驱？JF - European Respiratory Journal JO - Eur Respir J DO - 10.1183/13993003.03167-2020 VL - 56 IS - 4 SP - 2003167 AU - Eapen, Mathew Suji AU - Lu, Wenying AU - Gaikwad, Archana Vijay AU - Bhattarai, Prem AU -Chia，Collin au -Hardikar，Ashutosh au-豪格，Greg au -Sohal，Sukhwinder Singh Y1-2020/10/01 UR -http：//www.qdcxjkg.com/content.com/content/56/4/4/4/4/2003167.Abstract N2- ABSTRACT N2-ABSTRACT N2-兴趣阅读Huertas等人最近的社论。[1]，强调了内皮细胞功能障碍在严重急性呼吸道综合征2（SARS-COV-2）感染中的重要性。作者做出了一些非常引人入胜的见解，我们想进一步进行讨论，尤其是强调内皮细胞在启动感染后肺纤维化和血管重塑中的作用。血管紧张素转换酶2（ACE2）被认为是介导SARS-COV-2进入宿主细胞的主要受体。除了ACE2之外，其他促进SARS-COV-2进入的主要参与者包括跨膜丝氨酸蛋白酶2（TMPRSS2），FURIN，唾液酸和细胞外基质基质金属蛋白酶诱导剂（CD147）[1]。在他们的文章中，作者提供了一项研究的引人注目的综合，该研究比较了死于2019年冠状病毒病（COVID-19），急性呼吸窘迫综合征的患者的尸体肺组织，急性呼吸窘迫综合征（H1N1）感染以及年龄匹配的，年龄匹配的人，未感染的对照肺[1，2]。 A crucial inference was the connections between the significant increase in ACE2 positive endothelial cells and the substantial change in endothelial cell morphology, disruption of intercellular junctions, cell swelling, and the breakdown of the underlying basement membrane, all indicative of vascular structural modification in tune to the process of endothelial to mesenchymal transition (EndMT) [3]. Considering the implications for post-COVID-19 pulmonary fibrosis and vascular destruction seen in this infectious pathology, we believe that the role of EndMT in disease manifestation could be consequential.Endothelial to mesenchymal transition (EndMT) could lead to post-COVID-19 pulmonary fibrosis and vascular remodelling https://bit.ly/2QqSKxTClifford Craig Foundation Launceston General Hospital, Lung Foundation Australia, The Alfred Hospital Melbourne and James Hogg Lung Registry, The University of British Columbia, Canada. ER -