Evidence map›Paper›PMID 30211629›Full record

ArticleAmerican journal of respiratory and critical care medicine2019

Toll-like Receptor 3 Is a Therapeutic Target for Pulmonary Hypertension.

Daniela Farkas, A A Roger Thompson, Aneel R Bhagwani, Schuyler Hultman, Hyun Ji, Naveen Kotha, Grant Farr, Nadine D Arnold, Adam Braithwaite, Helen Casbolt and 7 more

Abstract read
In one paragraph

Article in American journal of respiratory and critical care medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 66 citations in OpenAlex.

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  20. Pattern recognition receptors in health and diseases.Signal transduction and targeted therapy · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 5 institutions in 2 countries.

Daniela Farkas1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
A A Roger Thompson2 Department of Infection, Immunity & Cardiovascular Disease, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, United Kingdom.
Aneel R Bhagwani1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
Schuyler Hultman1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
Hyun Ji1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
Naveen Kotha1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
Grant Farr1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.
Nadine D Arnold2 Department of Infection, Immunity & Cardiovascular Disease, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, United Kingdom.
Adam Braithwaite2 Department of Infection, Immunity & Cardiovascular Disease, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, United Kingdom.
Helen Casbolt2 Department of Infection, Immunity & Cardiovascular Disease, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, United Kingdom.
Jennifer E Cole3 Kennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.
Ian Sabroe2 Department of Infection, Immunity & Cardiovascular Disease, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, United Kingdom.
Claudia Monaco3 Kennedy Institute of Rheumatology, University of Oxford, Oxford, United Kingdom.
Carlyne D Cool4 Department of Pathology, University of Colorado Denver, Denver, Colorado; and.
Elena A Goncharova5 Pittsburgh Heart, Lung and Blood Vascular Medicine Institute, Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, and.
Allan Lawrie2 Department of Infection, Immunity & Cardiovascular Disease, Faculty of Medicine, Dentistry & Health, University of Sheffield, Sheffield, United Kingdom.
Laszlo Farkas1 Division of Pulmonary Disease and Critical Care Medicine, Department of Internal Medicine, Virginia Commonwealth University, Richmond, Virginia.ORCID 0000-0003-3772-470X
Virginia Commonwealth University · USUniversity of Sheffield · GBUniversity of Oxford · GBUniversity of Colorado Denver · USUniversity of Pittsburgh · US

Funding

Virus Vector Shared ResourceP30CA016059 · NCI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Keri R Maher · 1985 to 2026
$51.0M
Vascular Subphenotypes of Lung DiseaseP01HL103455 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI GLADWIN, MARK T · 2011 to 2020
$26.1M
Pulmonary Hypertension Breakthrough InitiativeR24HL123767 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI ALDRED, MICHEALA A, ERZURUM, SERPIL C. · 2014 to 2017
$10.1M
Regulation and Function of RAB7 in the pulmonary endotheliumR01HL139881 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI Laszlo Farkas · 2019 to 2026
$3.8M
Central role of endothelial stem cells in pulmonary arterial hypertensionR21HL123044 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FARKAS, LASZLO, FREISHTAT, ROBERT J · 2016 to 2017
$454k
Precursor cells in human pulmonary hypertensionR03HL114816 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI FARKAS, LASZLO · 2012 to 2013
$146k
British Heart Foundation FS/13/48/30453British Heart Foundation FS/18/13/33281British Heart Foundation PG/11/46/28979British Heart Foundation PG/18/1/33430British Heart Foundation PG/19/41/34426NCI NIH HHS P30 CA016059NHLBI NIH HHS P01 HL103455NHLBI NIH HHS R01 HL139881NHLBI NIH HHS R03 HL114816NHLBI NIH HHS R21 HL123044NHLBI NIH HHS R24 HL123767
6 · The paper itself

Abstract

rationalePulmonary arterial hypertension (PAH) is characterized by vascular cell proliferation and endothelial cell apoptosis. TLR3 (Toll-like receptor 3) is a receptor for double-stranded RNA and has been recently implicated in vascular protection.

objectivesTo study the expression and role of TLR3 in PAH and to determine whether a TLR3 agonist reduces pulmonary hypertension in preclinical models.

methodsLung tissue and endothelial cells from patients with PAH were investigated by polymerase chain reaction, immunofluorescence, and apoptosis assays. TLR3 MEASUREMENTS AND MAIN

resultsTLR3 expression was reduced in PAH patient lung tissue and endothelial cells, and TLR3

conclusionsOur work identifies a novel role for TLR3 in PAH based on the findings that reduced expression of TLR3 contributes to endothelial apoptosis and pulmonary vascular remodeling.

Indexed as

AnimalsDisease Models, AnimalHumansHypertension, PulmonaryLungMiceRatsSignal TransductionToll-Like Receptor 3Toll-Like Receptor 3apoptosisdouble-stranded RNAendothelial cellpulmonary hypertensiontoll-like receptor 3

Identifiers

PMID30211629
PMCPMC6353001
OpenAlexW2890682818

What OpenQuestion holds

Textmetadata
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.