key: cord-0749187-240z03f7 authors: Wu, Zhiyong; Hu, Rui; Zhang, Cuizhen; Ren, Wei; Yu, Anfeng; Zhou, Xiaoyang title: Elevation of plasma angiotensin II level is a potential pathogenesis for the critically ill COVID-19 patients date: 2020-06-05 journal: Crit Care DOI: 10.1186/s13054-020-03015-0 sha: af9b6be4687bf3a80fd9039a54816ec72a4c0ec4 doc_id: 749187 cord_uid: 240z03f7 nan critically ill COVID-19 patients and control (Fig. 1 ). These indicated that plasma Ang II elevation was closely related to the SARS-CoV-2 infection, which may be triggered by the interaction between S protein and ACE2 [1, 2] . This played important roles in COVID-19 progression. Previous study showed that subcutaneous Ang II infusion using osmotic pumps for 3 days led to decline of oxygenation and obvious pulmonary injuries after infusion of Ang II for 1 week [3] . For the mechanism, Ang II could promote apoptosis and skeleton reconstruction of pulmonary microvascular endothelial cells, hampering pulmonary microvascular endothelial barrier and the subsequent elevation of pulmonary exudate. This was extremely similar with the quarantine period and pathological manifestations of COVID-19 [4, 5] . Previous study [3] indicated that IL-22 could attenuate Ang II-induced pulmonary injury through modulating JAK2/STAT3 signaling pathway, which may provide new options for treating COVID-19. Therefore, elevation of Ang II triggered by interaction between ACE2 and S protein of SARS-CoV-2 may be important pathogenic factors for critically ill COVID-19 patients. Abbreviations SARS-CoV-2: Severe acute respiratory syndrome coronavirus 2; COVID-19: Coronavirus disease 2019; Ang II: Angiotensin II; RAS: Renin angiotensin system; ACE2: Angiotensin-converting enzyme 2 Fig. 1 The positive rate and concentration of plasma renin and Ang II in different groups. a There were no statistical differences in the concentration of renin in patients with different severity of COVID-19. b The plasma Ang II concentration in the critically ill COVID-19 cases and severe COVID-19 cases was significantly higher than that of the mild COVID-19 cases. c, d The renin and Ang II positive rate in the three groups showed no statistical difference. e There was no statistical difference in the concentration of renin in patients with critically ill COVID-19 compared with the control. f The plasma Ang II concentration in the critically ill COVID-19 cases was significantly higher than that of control. g The renin positive rate in the two groups showed no statistical difference. h The plasma Ang II positive rate in the critically ill COVID-19 cases was significantly higher than that of control. Control: critically ill non-COVID-19 cases. *P < 0.05, **P < 0.01 Receptor recognition by the novel coronavirus from Wuhan: an analysis based on decade-long structural studies of SARS coronavirus A pilot clinical trial of recombinant human angiotensin-converting enzyme 2 in acute respiratory distress syndrome Interleukin 22 attenuated angiotensin II induced acute lung injury through inhibiting the apoptosis of pulmonary microvascular endothelial cells COVID-19 and the RAAS-a potential role for angiotensin II? VE-cadherin involved in the pulmonary microvascular endothelial cell barrier injury induced by angiotensin II through modulating the cellular apoptosis and skeletal rearrangement Publisher's Note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations Not applicable. The datasets used and analyzed during the current study are available from the corresponding author on reasonable request.Ethics approval and consent to participate All studies were approved by the Ethical Committee of Renmin Hospital of Wuhan University. Each patient signed the informed consent. The authors declare that they have no competing interests.Received: 8 May 2020 Accepted: 21 May 2020