PMC:7029759 / 25424-26887 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7029759","sourcedb":"PMC","sourceid":"7029759","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7029759","text":"An additional advantage of using ACE2 as a 2019-nCoV S protein neutralizing agent is that ACE2 administration could also directly treat the pneumonia pathophysiology. A portion of patients with SARS and 2019-nCoV infection develop pneumonia, which is characterized by pulmonary edema and acute respiratory distress syndrome (ARDS) 1, 2. The viruses may, in part, cause ARDS through viral-induced ACE2 protein shedding and ACE2 protein decreased expression, both of which are mediated by S protein binding 54. Administration of recombinant ACE2 protein has been shown to improve acute lung injury through decreasing angiotensin II levels and the hormones subsequent binding to angiotensin II type 1a receptor 57. Recombinant ACE2 can also reduce ARDS in respiratory syncytial virus 58 and H5N1 influenza 59 infection models. Based on these promising preclinical studies, recombinant human ACE2 (rhACE2) was moved into clinical trials in order to treat ARDS in critically ill patients. A phase I trial demonstrated rhACE2 was well tolerated with no effects seen on the cardiovascular system 60. A phase II trial demonstrated on-target efficacy in reducing Ang1-8 peptide levels, but did not show significant modulation of respiratory parameters 61. It remains to be seen whether rhACE2 administration has the same clinical benefits in treating ARDS that have been seen in animal models, and whether ACE2-Fc administration could alleviate ARDS in 2019-nCoV 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