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Infection of lung cells by the corona virus results in a loss of the balance between, on the one hand, angiotensin II-mediated stimulation of the angiotensin II type 1 receptor and, on the other hand, stimulation of the angiotensin II type 2 receptor and/or the Mas receptor. The unbalanced enhanced stimulation of the angiotensin II type 1 receptor causes inflammation, edema and contributes to the pathogenesis of severe acute respiratory distress syndrome. Here we hypothesize that stable, receptor-specific agonists of the angiotensin II type 2 receptor and of the Mas receptor are molecular medicines to treat COVID-19 patients. These agonists have therapeutic potential in the acute disease but in addition may reduce COVID-19-associated long-term pulmonary dysfunction and overall end-organ damage of this disease.
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?:doi
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10.1186/s10020-020-00211-0
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document_parses/pdf_json/2ecda4f1df5c5d08ae3f908b588426cb40b281af.json
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document_parses/pmc_json/PMC7430134.xml.json
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?:title
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Does activation of the protective Renin-Angiotensin System have therapeutic potential in COVID-19?
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