Kallikrein-kinin blockade in patients with COVID-19 to prevent acute respiratory distress syndrome
- Departments of Internal Medicine, Radboudumc Center for Infectious Diseases (RCI), Radboudumc, Netherlands
- Department for Genomics and Immunoregulation, Life and Medical Sciences Institute (LIMES), University of Bonn, Germany
- Department of Pharmacy, Radboudumc Center for Infectious Diseases (RCI), Radboudumc, Netherlands
- Intensive Care, Radboudumc Center for Infectious Diseases (RCI), Radboudumc, Netherlands
Figures
Figure 1
The kinin-kallikrein system and ACE/ACE2.
The pathways of processing of low-molecular-weight kininogen (LMWK) and high-molecular-weight kallikrein (HMWK) leading to Bradykinin 1 (B1) receptor agonists and Bradykinin 2 (B2) receptor agonists. CPM = carboxypeptidaseM; CPN = carboxypeptidaseN.
Figure 2
Schematic view of treatment strategies in COVID-19.
Figure 3
Alveolus in normal setting and during moderate and severe COVID-19, (A) normal, (B) mild inflammation, (C) hyperinflammation.
ACE2 downregulation by the SARS-CoV-2 is followed by loss of neutralizing capacity of Lys-des-arg9-bradykinin (BK) in the lung leading to plasma leakage. Subsequently plasma leakage results in more B1R ligands (des-arg9-BK) and B2R ligands (bradykinin).
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Kallikrein-kinin blockade in patients with COVID-19 to prevent acute respiratory distress syndrome
eLife 9:e57555.
https://doi.org/10.7554/eLife.57555
