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• W3048430059 abstract "To date the pathophysiology of COVID-19 remains unclear: this represents a factor determining the current lack of effective treatments. In this paper we hypothesized a complex host response to SARS-CoV-2, with the Contact System (CS) playing a pivotal role in innate immune response. CS is linked with different proteolytic defense systems operating in human vasculature: the Kallikrein-Kinin (KKS), the Coagulation/Fibrinolysis and the Renin-Angiotensin (RAS) Systems. We investigated the role of the mediators involved. CS consists of Factor XII (FXII) and plasma prekallikrein (complexed to high-molecular-weight kininogen-HK). Autoactivation of FXII by contact with SARS-CoV-2 could lead to activation of intrinsic coagulation, with fibrin formation (microthrombosis), and fibrinolysis, resulting in increased D-dimer levels. Activation of kallikrein by activated FXII leads to production of bradykinin (BK) from HK. BK binds to B2-receptors, mediating vascular permeability, vasodilation and edema. B1-receptors, binding the metabolite [des-Arg9]-BK (DABK), are up-regulated during infections and mediate lung inflammatory responses. BK could play a relevant role in COVID-19 as already described for other viral models. Angiotensin-Converting-Enzyme (ACE) 2 displays lung protective effects: it inactivates DABK and converts angiotensin II (Ang II) into Angiotensin-(1-7) and angiotensin I into Angiotensin-(1-9). SARS-CoV-2 binds to ACE2 for cell entry, downregulating it: an impaired DABK inactivation could lead to an enhanced activity of B1-receptors, and the accumulation of Ang II, through a negative feedback loop, may result in decreased ACE activity, with consequent increase of BK. Therapies targeting the CS, the KKS and action of BK could be effective for the treatment of COVID-19." @default.
• W3048430059 created "2020-08-18" @default.
• W3048430059 creator A5006739688 @default.
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• W3048430059 date "2020-08-11" @default.
• W3048430059 modified "2023-10-18" @default.
• W3048430059 title "Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?" @default.
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• W3048430059 doi "https://doi.org/10.3389/fimmu.2020.02014" @default.
• W3048430059 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7432138" @default.
• W3048430059 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32849666" @default.
• W3048430059 hasPublicationYear "2020" @default.
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