About: Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key? Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?
Creator	Liu, Zhenlong Zanichelli, Andrea Iuri, Federico Meini, Simone Roberts, Anna Sbrojavacca, Rodolfo Suffritti, Chiara Tascini, Carlo Preissner, Klaus
Source	Medline; PMC
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-Arg(9)]-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.
has issue date	2020-08-11(xsd:dateTime)
bibo:doi	10.3389/fimmu.2020.02014
bibo:pmid	32849666
has license	cc-by
sha1sum (hex)	40346bbf2b57559e7ceb1a6648df3823187ea0f3
schema:url	https://doi.org/10.3389/fimmu.2020.02014
resource representing a document's title	Understanding the Pathophysiology of COVID-19: Could the Contact System Be the Key?
has PubMed Central identifier	PMC7432138
has PubMed identifier	32849666
schema:publication	Front Immunol
resource representing a document's body	covid:40346bbf2b57559e7ceb1a6648df3823187ea0f3#body_text
is schema:about of	named entity 'Understanding' named entity 'Key' named entity 'Pathophysiology' named entity 'COVID-19' named entity 'coagulation' named entity 'histopathological' named entity 't-PA' named entity 'evolution' named entity 'ACE2' named entity 'lung' named entity 'bradykinin' named entity 'coagulation' named entity 'ARBs' named entity 'eukaryotic' named entity 'wild-type' named entity 'hyperplasia' named entity 'pharmacological' named entity 'hemostasis' named entity 'positive feedback loop' named entity 'signaling pathways' named entity 'carboxypeptidase' named entity 'coagulation' named entity 'histamine' named entity 'ACE' named entity 'extracellular RNA' named entity 'peptide hormone' named entity 'plasma' named entity 'ACE-inhibitors' named entity 'plasmin' named entity 'coagulation' named entity 'ACE2' named entity 'alveolar' named entity 'etiology' named entity 'RAS' named entity 'plasma' named entity 'conformational change' named entity 'hantavirus' named entity 'trans-membrane domain' named entity 'Type 1' named entity 'receptor' named entity 'mice' named entity 'peptidase' named entity 'CRP' named entity 'KKS' named entity 'COVID' named entity 'nitric oxide synthase' named entity 'inflammatory response' named entity 'coagulation' named entity 'innate immune' named entity 'coagulation' named entity 'evolution' named entity 'necrosis' named entity 'C-reactive protein' named entity 'dry cough' named entity 'COVID-19' named entity 'RAS' named entity 'Angiotensin' named entity 'enterocytes' named entity 'lactate dehydrogenase' named entity 'Renin' named entity 'D-dimer' named entity 'edema' named entity 'Angiotensin II' named entity 'pharmacologically' named entity 'RAS' named entity 'SARS-CoV-2' named entity 'Ang II' named entity 'endosomal' named entity 'protease inhibitory' named entity 'cytokines' named entity 'pneumocyte' named entity 'chloroquine' named entity 'coronaviruses'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2025 OpenLink Software