About: The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin

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

About: The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system
Creator	Montijn, Roy Offringa, Annette Paul, Martin Pinto, Yigal Pinto-Sietsma, Sara-Joan Singh, Sandeep Cardiology, Amsterdam Umc,
Source	Medline; PMC
abstract	The SARS-CoV-2 pandemic is a healthcare crisis caused by insufficient knowledge applicable to effectively combat the virus. Therefore, different scientific discovery strategies need to be connected, to generate a rational treatment which can be made available as rapidly as possible. This relies on a solid theoretical understanding of the mechanisms of SARS-CoV-2 infection and host responses, which is coupled to the practical experience of clinicians that are treating patients. Because SARS-CoV-2 enters the cell by binding to angiotensin-converting enzyme 2 (ACE2), targeting ACE2 to prevent such binding seems an obvious strategy to combat infection. However, ACE2 performs its functions outside the cell and was found to enter the cell only by angiotensin II type 1 receptor (AT1R)-induced endocytosis, after which ACE2 is destroyed. This means that preventing uptake of ACE2 into the cell by blocking AT1R would be a more logical approach to limit entry of SARS-CoV-2 into the cell. Since ACE2 plays an important protective role in maintaining key biological processes, treatments should not disrupt the functional capacity of ACE2, to counterbalance the negative effects of the infection. Based on known mechanisms and knowledge of the characteristics of SARS-CoV we propose the hypothesis that the immune system facilitates SARS-CoV-2 replication which disrupts immune regulatory mechanisms. The proposed mechanism by which SARS-CoV-2 causes disease immediately suggests a possible treatment, since the AT1R is a key player in this whole process. AT1R antagonists appear to be the ideal candidate for the treatment of SARS-CoV-2 infection. AT1R antagonists counterbalance the negative consequences of angiotesnin II and, in addition, they might even be involved in preventing the cellular uptake of the virus without interfering with ACE2 function. AT1R antagonists are widely available, cheap, and safe. Therefore, we propose to consider using AT1R antagonists in the treatment of SARS-CoV-2.
has issue date	2020-05-28(xsd:dateTime)
bibo:doi	10.1093/ehjcvp/pvaa053
bibo:pmid	32464637
has license	cc-by-nc
sha1sum (hex)	820cf100aabf6364430a4bf742c875be93134dc6
schema:url	https://doi.org/10.1093/ehjcvp/pvaa053
resource representing a document's title	The mechanistic overview of SARS-CoV-2 using angiotensin-converting enzyme 2 to enter the cell for replication: possible treatment options related to the renin–angiotensin system
has PubMed Central identifier	PMC7314063
has PubMed identifier	32464637
schema:publication	Eur Heart J Cardiovasc Pharmacother
resource representing a document's body	covid:820cf100aabf6364430a4bf742c875be93134dc6#body_text
is schema:about of	named entity 'TARGETING' named entity 'STRATEGIES' named entity 'GENERATE' named entity 'THE CELL' named entity 'INFECTION' named entity 'INTERFERING' named entity 'CANDIDATE' named entity 'TREATMENTS' named entity 'NEED' named entity 'cellular uptake' named entity 'infection' named entity 'type 1' named entity 'infection' named entity 'SARS-CoV-2' named entity 'ACE2' named entity 'angiotensin-converting enzyme 2' named entity 'endosome' named entity 'ACE2' named entity 'hypoxia' named entity 'viral replication' named entity 'ARBs' named entity 'metabolites' named entity 'COVID' named entity 'pulmonary infection' named entity 'type 1' named entity 'T-cell' named entity 'virus' named entity 'virus' named entity 'ACE2' named entity 'ACE2' named entity 'ACE2' named entity 'ACE2' named entity 'AT1R' named entity 'inflammation' named entity 'acute kidney injury' named entity 'chloroquine' named entity 'ACE2' named entity 'infection' named entity 'endocytosis' named entity 'chloroquine' named entity 'nucleic acids' named entity 'ACE2' named entity 'SARS-CoV-2' named entity 'ACE2' named entity 'SARS-CoV' named entity 'AT1R' named entity 'interleukin-6' named entity 'intestine' named entity 'infection' named entity 'SARS-CoV-2' named entity 'cell surface' named entity 'inflammation' named entity 'innate immune response' named entity 'ACE2' named entity 'homeostatic' named entity 'virus' named entity 'vasoconstriction' named entity 'placebo' named entity 'cell membrane' named entity 'AT1R' named entity 'ACE2' named entity 'ACE2' named entity 'COVID' named entity 'cytoplasm' named entity 'ACE2' named entity 'ACEIs' named entity 'proinflammatory' named entity 'nitric oxide' named entity 'infection' named entity 'ACE2' named entity 'ACE2' named entity 'viral life cycle' named entity 'vasoconstriction' named entity 'ACE2'

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 © 2009-2024 OpenLink Software