Evidence map›Paper›PMID 33375371›Full record

ReviewViruses2020

Endothelium Infection and Dysregulation by SARS-CoV-2: Evidence and Caveats in COVID-19.

Isabelle Bernard, Daniel Limonta, Lara K Mahal, Tom C Hobman

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Viruses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 109 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
109citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

109 citing papers in PubMed, 1 synthesis or guideline pooled it, 179 citations in OpenAlex.

  1. Pooled it
  2. Three-Day Icatibant on Top of Standard Care in Patients With Coronavirus Disease 2019 Pneumonia: A Randomized, Open-Label, Phase 2, Proof-of-Concept Trial.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
    Trial
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49 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Isabelle BernardDepartment of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, Canada.
Daniel LimontaDepartment of Cell Biology, University of Alberta, Edmonton, AB T6G 2H7, Canada.ORCID 0000-0002-5128-6542
Lara K MahalDepartment of Chemistry, University of Alberta, Edmonton, AB T6G 2G2, Canada.
Tom C HobmanDepartment of Medical Microbiology & Immunology, University of Alberta, Edmonton, AB T6G 2E1, Canada.
University of Alberta · CA

Funding

CIHR OV3-172302CIHR PJT-148699CIHR PJT-162417
6 · The paper itself

Abstract

The ongoing pandemic of coronavirus disease 2019 (COVID-19) caused by the acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) poses a persistent threat to global public health. Although primarily a respiratory illness, extrapulmonary manifestations of COVID-19 include gastrointestinal, cardiovascular, renal and neurological diseases. Recent studies suggest that dysfunction of the endothelium during COVID-19 may exacerbate these deleterious events by inciting inflammatory and microvascular thrombotic processes. Although controversial, there is evidence that SARS-CoV-2 may infect endothelial cells by binding to the angiotensin-converting enzyme 2 (ACE2) cellular receptor using the viral Spike protein. In this review, we explore current insights into the relationship between SARS-CoV-2 infection, endothelial dysfunction due to ACE2 downregulation, and deleterious pulmonary and extra-pulmonary immunothrombotic complications in severe COVID-19. We also discuss preclinical and clinical development of therapeutic agents targeting SARS-CoV-2-mediated endothelial dysfunction. Finally, we present evidence of SARS-CoV-2 replication in primary human lung and cardiac microvascular endothelial cells. Accordingly, in striving to understand the parameters that lead to severe disease in COVID-19 patients, it is important to consider how direct infection of endothelial cells by SARS-CoV-2 may contribute to this process.

Indexed as

ADAM17 ProteinAngiotensin-Converting Enzyme 2Antiviral AgentsCoronavirusCoronavirus InfectionsCOVID-19Endothelial CellsEndotheliumEndothelium, VascularHumansLungSARS-CoV-2ThrombosisVirus ReplicationACE2 protein, humanADAM17 ProteinADAM17 protein, humanAngiotensin-Converting Enzyme 2Antiviral AgentsACE2ADAM17bradykinin–kallikrein pathwayCOVID-19endothelial dysfunctionimmunothrombosispericyteRAASSARS-CoV-2therapeutics

Identifiers

PMID33375371
PMCPMC7823949
OpenAlexW3118061239

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.