A lesson from a saboteur: High‐MW kininogen impact in coronavirus‐induced disease 2019
Chiara Colarusso, Michela Terlizzi, Aldo Pinto, Rosalinda Sorrentino
Abstract
The newly identified coronavirus SARS‐CoV‐2 that spread from China is causing the pandemic COVID‐19 with a fatality rate from 5‐15%. It causes fever, cough, myalgia, fatigue up to dyspnoea, responsible for hospitalization and artificial oxygenation. SARS‐CoV‐2 infects human cells using ACE2, the transmembrane protease serine 2 (TMPRSS2) and the SARS‐CoV‐2 main protease (M pro ). Once bound to ACE2 and the other two proteases in concert they allow the virus replication and spread throughout the body. Our attention has been focused on the role of ACE2 as its binding to by the virus increases bradykinin and its metabolites, which facilitate inflammation in the lung (causing cough and fever), coagulation and the complement system. These three systems are involved in angioedema, cardiovascular dysfunction and sepsis, pathologies which occur in COVID‐19 patients. Thus, we propose that blocking the kallikrein–kinin system with lanadelumab, approved for hereditary angioedema, will prevent facilitation of these 3 systems. Linked Articles This article is part of a themed issue on The Pharmacology of COVID‐19. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v177.21/issuetoc