| First Author | van de Veerdonk FL | Year | 2020 |
| Journal | Elife | Volume | 9 |
| PubMed ID | 32338605 | Mgi Jnum | J:291465 |
| Mgi Id | MGI:6443107 | Doi | 10.7554/eLife.57555 |
| Citation | van de Veerdonk FL, et al. (2020) Kallikrein-kinin blockade in patients with COVID-19 to prevent acute respiratory distress syndrome. Elife 9:e57555 |
| abstractText | COVID-19 patients can present with pulmonary edema early in disease. We propose that this is due to a local vascular problem because of activation of bradykinin 1 receptor (B1R) and B2R on endothelial cells in the lungs. SARS-CoV-2 enters the cell via ACE2 that next to its role in RAAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the B1R. Without ACE2 acting as a guardian to inactivate the ligands of B1R, the lung environment is prone for local vascular leakage leading to angioedema. Here, we hypothesize that a kinin-dependent local lung angioedema via B1R and eventually B2R is an important feature of COVID-19. We propose that blocking the B2R and inhibiting plasma kallikrein activity might have an ameliorating effect on early disease caused by COVID-19 and might prevent acute respiratory distress syndrome (ARDS). In addition, this pathway might indirectly be responsive to anti-inflammatory agents. |
