Evidence map›Paper›PMID 32210969›Full record

ArticleFrontiers in immunology2020

Prominence of IL6, IGF, TLR, and Bioenergetics Pathway Perturbation in Lung Tissues of Scleroderma Patients With Pulmonary Fibrosis.

Ludivine Renaud, Willian A da Silveira, Naoko Takamura, Gary Hardiman, Carol Feghali-Bostwick

Open access · goldAbstract readComparative Study
In one paragraph

Article in Frontiers in immunology, 2020. 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
4.9field-weighted citation impact, top 4% 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, 58 citations in OpenAlex.

  1. Article
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  8. Review
  9. Revealing the impact ofFrontiers in immunology · 2025
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  15. Searching for an Animal Model with Clinical Features of Scleroderma.American journal of respiratory cell and molecular biology · 2023
    Article
  16. Article
  17. Article
  18. The Role of SOX9 in IGF-II-Mediated Pulmonary Fibrosis.International journal of molecular sciences · 2023
    Article
  19. Review
  20. Article
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

5 authors at 2 institutions in 2 countries.

Ludivine RenaudDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Willian A da SilveiraSchool of Biological Sciences, Institute for Global Food Security, Queens University Belfast, Belfast, United Kingdom.
Naoko TakamuraDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Gary HardimanDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Carol Feghali-BostwickDepartment of Medicine, Medical University of South Carolina, Charleston, SC, United States.
Medical University of South Carolina · USQueen's University Belfast · GB

Funding

The Genetic Basis of Opioid Dependence Vulnerablility in a Rodent ModelU01DA045300 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Christine Cheng, Dongjun Chung · 2018 to 2026
$6.1M
Training Grant in Inflammatory and Fibrosing DiseasesT32AR050958 · NIAMS · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI DIANE L KAMEN · 2005 to 2026
$4.2M
Mechanism of Action of Anti-Fibrotic PeptideR01HL121262 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI FEGHALI-BOSTWICK, CAROL A. · 2017 to 2020
$1.5M
Scleroderma Twin Study and analysis of Estrogen in patients with dcSScK24AR060297 · NIAMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FEGHALI-BOSTWICK, CAROL A. · 2013 to 2025
$1.4M
NHLBI NIH HHS R01 HL121262NIAMS NIH HHS K24 AR060297NIAMS NIH HHS T32 AR050958NIDA NIH HHS U01 DA045300
6 · The paper itself

Abstract

Scleroderma-associated pulmonary fibrosis (SSc-PF) and idiopathic pulmonary fibrosis (IPF) are two of many chronic fibroproliferative diseases that are responsible for nearly 45% of all deaths in developed countries. While sharing several pathobiological characteristics, they also have very distinct features. Currently no effective anti-fibrotic treatments exist that can halt the progression of PF or reverse it. Our goal is to uncover potential gene targets for the development of anti-fibrotic therapies efficacious in both diseases, and those specific to SSc-PF, by identifying universal pathways and molecules driving fibrosis in SSc-PF and IPF tissues as well as those unique to SSc-PF. Using DNA microarray data, a meta-analysis of the differentially expressed (DE) genes in SSc-PF and IPF lung tissues (diseased vs. normal) was performed followed by a full systems level analysis of the common and unique transcriptomic signatures obtained. Protein-protein interaction networks were generated to identify hub proteins and explore the data using the centrality principle. Our results suggest that therapeutic strategies targeting IL6 trans-signaling,

Indexed as

BasidiomycotaDisease ProgressionEnergy MetabolismHomeostasisHumansIdiopathic Pulmonary FibrosisInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor IInterleukin-6LungMycosesOligonucleotide Array Sequence AnalysisSignal TransductionToll-Like ReceptorsTranscriptomeIGFBP2 protein, humanInsulin-Like Growth Factor Binding Protein 2Insulin-Like Growth Factor IInterleukin-6Toll-Like Receptorsidiopathicinterstitial lung diseasemicroarraypulmonary fibrosissclerodermasystemic sclerosis

Identifiers

PMID32210969
PMCPMC7075854
OpenAlexW3011090345

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.