Evidence map›Paper›PMID 28390872›Full record

ReviewAntiviral research2017

The role of epidermal growth factor receptor (EGFR) signaling in SARS coronavirus-induced pulmonary fibrosis.

Thiagarajan Venkataraman, Matthew B Frieman

Registry-linked trialAbstract readReview
In one paragraph

Review in Antiviral research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05386485 (FUNCTION Study), which is not on this map. Cited by 116 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
116citing papers in PubMed, 2 pooled it
11.7field-weighted citation impact, top 1% 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.

NCT05386485 unknown statusnot on this mapstarted 2021, after this paper: background citation

FUNCTION Study: Follow- Up Study iN SARS-CoV-2 infecTION. Long-term Impact on Cardiopulmonary Function and Quality of Life in Patients Recovered From SARS-CoV-2 Infection in Lima, Peru

TypeobservationalSponsorUniversidad Peruana Cayetano HerediaRan2021 to 2022Enrolled162ConditionsCOVID-19ArmsNone intervation
3 · Its place in the literature

Who cites it

116 citing papers in PubMed, 2 syntheses or guidelines pooled it, 195 citations in OpenAlex.

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56 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

2 authors at 1 institution in 1 country.

Thiagarajan VenkataramanDepartment of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St. Room 380, Baltimore, MD, 21201, USA.
Matthew B FriemanDepartment of Microbiology and Immunology, University of Maryland at Baltimore, 685 West Baltimore St. Room 380, Baltimore, MD, 21201, USA. Electronic address: mfrieman@som.umaryland.edu.
University of Maryland, Baltimore · US

Funding

Signaling Pathways in Innate ImmunityT32AI095190 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI Stefanie N. Vogel · 2012 to 2026
$4.7M
Role of the Epithelial Growth Factor Receptor in SARS Coronavirus PathogenesisR01AI095569 · NIAID · UNIVERSITY OF MARYLAND BALTIMORE · PI FRIEMAN, MATTHEW BRYAN · 2011 to 2016
$2.3M
NIAID NIH HHS R01 AI095569NIAID NIH HHS T32 AI095190
6 · The paper itself

Abstract

Many survivors of the 2003 outbreak of severe acute respiratory syndrome (SARS) developed residual pulmonary fibrosis with increased severity seen in older patients. Autopsies of patients that died from SARS also showed fibrosis to varying extents. Pulmonary fibrosis can be occasionally seen as a consequence to several respiratory viral infections but is much more common after a SARS coronavirus (SARS-CoV) infection. Given the threat of future outbreaks of severe coronavirus disease, including Middle East respiratory syndrome (MERS), it is important to understand the mechanisms responsible for pulmonary fibrosis, so as to support the development of therapeutic countermeasures and mitigate sequelae of infection. In this article, we summarize pulmonary fibrotic changes observed after a SARS-CoV infection, discuss the extent to which other respiratory viruses induce fibrosis, describe available animal models to study the development of SARS-CoV induced fibrosis and review evidence that pulmonary fibrosis is caused by a hyperactive host response to lung injury mediated by epidermal growth factor receptor (EGFR) signaling. We summarize work from our group and others indicating that inhibiting EGFR signaling may prevent an excessive fibrotic response to SARS-CoV and other respiratory viral infections and propose directions for future research.

Indexed as

AnimalsDisease Models, AnimalErbB ReceptorsHost-Pathogen InteractionsHumansLung InjuryMicePathology, MolecularPulmonary FibrosisSevere Acute Respiratory SyndromeSevere acute respiratory syndrome-related coronavirusSignal TransductionWound HealingEGFR protein, mouseErbB ReceptorsEGFRFibrosisSARS-CoVWound healing

Identifiers

PMID28390872
PMCPMC5507769
OpenAlexW2605314287

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.