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{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7108679","sourcedb":"PMC","sourceid":"7108679","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7108679","text":"Finally, as clinician scientists, we realize that research and innovation will ultimately provide solutions to this crisis, whether through enhanced diagnostics, innovative therapies, or future vaccines. A potentially exciting endocrine-connected observation is the elucidation of the mechanism of entry of SARS-CoV-2 into cells. Here, angiotensin-converting enzyme 2 (ACE2) is now established as the SARS-CoV receptor (9) but with conflicting data as to its translational relevance. It has been suggested that angiotensin-converting enzyme inhibitors/angiotensin receptor blockers might increase susceptibility and severity to COVID-19 through upregulation of ACE2 and thereby possibly explain the overrepresentation of hypertensive patients in patients dying from COVID-19 (10). Upregulation of ACE2 might also explain the poor outcome in smokers versus nonsmokers, but it is important to stress that these are preliminary reports and should not result in changing prescribed medications at this stage (11). APN01 is a recombinant human ACE2 developed by APEIRON for the treatment of acute lung injury, acute respiratory distress syndrome, and pulmonary arterial hypertension; by slowing viral entry into cells and viral spread, it may be beneficial, and clinical trials are underway (12). Conversely, angiotensin II is known to stimulate alveolar epithelial cell apoptosis, and inhibition of this with angiotensin receptor 1 blockers such as losartan might reduce mortality from acute respiratory distress syndrome in COVID-19 infection (13).","tracks":[]}