TY - Jour T1 - 内皮对间充质转换：后Covid-19间质肺纤维化和血管抹除的前体？JF - 欧洲呼吸杂志Jo - Eur Respir J Do - 10.1183 / 13993003.03167-2020 VL - 56是 - 4 SP - 2003167 Au - Eapen，Mathew Suji Au - Lu，Wengy Au - Gaikwad，Archana Vijay Au - Bhattarai，Au -Chia，Collin Au - Hardikar，Ashutosh Au - Haug，Greg Au - Sohal，Sukhwinder Singh Y1 - 2020/10/01 Ur - //www.qdcxjkg.com/content/56/4/2003167.abstract n2 - 我们利息阅读近期霍尔塔等人的社论。[1]，突出了内皮细胞功能障碍在严重急性呼吸综合征冠状病毒2（SARS-COV-2）感染患者中的重要性。作者已经做出了一些非常令人迷人的见解，我们想进一步接受这一讨论，特别是强调内皮细胞在发起后肺纤维化和血管重塑中的作用。已经提出了血管紧张素转化酶2（ACE2）作为用于将SARS-COV-2进入宿主细胞的主要受体。除了ACE2之外，促进SARS-COV-2进入的另一个关键球员，包括跨膜丝氨酸蛋白酶2（TMPRSS2），Furin，唾液酸和细胞外基质金属蛋白酶诱导剂（CD147）[1]。在他们的文章中，提交人提供了从研究患者从冠状病毒疾病（Covid-19）的患者中的研究患者的研究令人兴奋的推动，这是由于流感A（H1N1）感染和从年龄匹配的那些，那么急性呼吸窘迫综合征。未感染的控制肺[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 -