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.
【저자키워드】 COVID-19, ACE2, ARDS, MasR, angiotensin, AT1R, AT2R, 【초록키워드】 Inflammation, Pathogenesis, virus, Medicine, edema, receptor, molecular, disease, COVID-19 patients, acute respiratory distress, therapeutic potential, syndrome, treat, agonist, pulmonary dysfunction, end-organ damage, lung cell, addition, contribute, cause, reduce, 【제목키워드】 Protective, Activation, therapeutic potential, System,