Abstract
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.
| Original language | English |
|---|---|
| Article number | 80 |
| Number of pages | 5 |
| Journal | Molecular medicine |
| Volume | 26 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 17-Aug-2020 |
Keywords
- COVID-19
- ARDS
- ACE2
- Angiotensin
- AT(1)R
- AT(2)R
- MasR
- PULMONARY-HYPERTENSION
- TYPE-2 RECEPTOR
- PROGRESSION