Evidence map›Paper›PMID 28655914›Full record

ArticleScientific reports2017

IGF1R deficiency attenuates acute inflammatory response in a bleomycin-induced lung injury mouse model.

Sergio Piñeiro-Hermida, Icíar P López, Elvira Alfaro-Arnedo, Raquel Torrens, María Iñiguez, Lydia Alvarez-Erviti, Carlos Ruíz-Martínez, José G Pichel

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

  1. Pooled it
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  16. Diabetes and COVID-19: The potential role of mTOR.Diabetes research and clinical practice · 2022
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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

8 authors at 2 institutions in 1 country.

Sergio Piñeiro-HermidaLung Cancer and Respiratory Diseases Unit, Centro de Investigación Biomédica de La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Icíar P LópezLung Cancer and Respiratory Diseases Unit, Centro de Investigación Biomédica de La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Elvira Alfaro-ArnedoLung Cancer and Respiratory Diseases Unit, Centro de Investigación Biomédica de La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Raquel TorrensLung Cancer and Respiratory Diseases Unit, Centro de Investigación Biomédica de La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
María IñiguezGenomics Core Facility, Centro de Investigación Biomédica de La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Lydia Alvarez-ErvitiMolecular Neurobiology Unit, Centro de Investigación Biomédica de la Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain.
Carlos Ruíz-MartínezPneumology Service, Hospital San Pedro, Logroño, Spain.
José G PichelLung Cancer and Respiratory Diseases Unit, Centro de Investigación Biomédica de La Rioja (CIBIR), Fundación Rioja Salud, Logroño, Spain. jgpichel@riojasalud.es.ORCID 0000-0001-8580-0952
Center for Biomedical Research of La Rioja · ESHospital San Pedro · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IGF1R (Insulin-like Growth Factor 1 Receptor) is a tyrosine kinase with pleiotropic cellular functions. IGF activity maintains human lung homeostasis and is implicated in pulmonary diseases such as cancer, ARDS, COPD, asthma and fibrosis. Here we report that lung transcriptome analysis in mice with a postnatally-induced Igf1r gene deletion showed differentially expressed genes with potentially protective roles related to epigenetics, redox and oxidative stress. After bleomycin-induced lung injury, IGF1R-deficient mice demonstrated improved survival within a week. Three days post injury, IGF1R-deficient lungs displayed changes in expression of IGF system-related genes and reduced vascular fragility and permeability. Mutant lungs presented reduced inflamed area, down-regulation of pro-inflammatory markers and up-regulation of resolution indicators. Decreased inflammatory cell presence in BALF was reflected in diminished lung infiltration mainly affecting neutrophils, also corroborated by reduced neutrophil numbers in bone marrow, as well as reduced lymphocyte and alveolar macrophage counts. Additionally, increased SFTPC expression together with hindered HIF1A expression and augmented levels of Gpx8 indicate that IGF1R deficiency protects against alveolar damage. These findings identify IGF1R as an important player in murine acute lung inflammation, suggesting that targeting IGF1R may counteract the inflammatory component of many lung diseases.

Indexed as

Acute Lung InjuryAnimalsBiomarkersBleomycinCapillary PermeabilityCell ProliferationDisease Models, AnimalGene ExpressionGene Expression ProfilingHypoxia-Inducible Factor 1, alpha SubunitInflammationMiceMice, KnockoutMice, TransgenicMutationReceptor, IGF Type 1BiomarkersBleomycinHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitReceptor, IGF Type 1

Identifiers

PMID28655914
PMCPMC5487362
OpenAlexW2659277361

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.