Evidence map›Paper›PMID 31952466›Full record

ArticleMolecular medicine (Cambridge, Mass.)2020

Identification of biomarkers in common chronic lung diseases by co-expression networks and drug-target interactions analysis.

Mazaher Maghsoudloo, Sadegh Azimzadeh Jamalkandi, Ali Najafi, Ali Masoudi-Nejad

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
5.4field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

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  20. Sex-specific associations of asthma acquisition with changes in DNA methylation during adolescence.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2021
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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

4 authors at 2 institutions in 3 countries.

Mazaher MaghsoudlooLaboratory of Systems Biology and Bioinformatics (LBB), Department of Bioinformatics, Kish International Campus, University of Tehran, Kish Island, Iran.
Sadegh Azimzadeh JamalkandiChemical Injuries Research Center, Systems Biology and Poisonings Institute, Tehran, Iran. azimzadeh@nigeb.ac.ir.
Ali NajafiMolecular Biology Research Center, Systems Biology and Poisonings Institute, Tehran, Iran.
Ali Masoudi-NejadLaboratory of Systems Biology and Bioinformatics (LBB), Department of Bioinformatics, Kish International Campus, University of Tehran, Kish Island, Iran. amasoudin@ut.ac.ir.ORCID 0000-0003-0659-5183
University of Tehran · IRIran Meteorological Organization · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundasthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF) are three serious pulmonary diseases that contain common and unique characteristics. Therefore, the identification of biomarkers that differentiate these diseases is of importance for preventing misdiagnosis. In this regard, the present study aimed to identify the disorders at the early stages, based on lung transcriptomics data and drug-target interactions.

methodsTo this end, the differentially expressed genes were found in each disease. Then, WGCNA was utilized to find specific and consensus gene modules among the three diseases. Finally, the disease-disease similarity was analyzed, followed by determining candidate drug-target interactions.

resultsThe results confirmed that the asthma lung transcriptome was more similar to COPD than IPF. In addition, the biomarkers were found in each disease and thus were proposed for further clinical validations. These genes included RBM42, STX5, and TRIM41 in asthma, CYP27A1, GM2A, LGALS9, SPI1, and NLRC4 in COPD, ATF3, PPP1R15A, ZFP36, SOCS3, NAMPT, and GADD45B in IPF, LRRC48 and CETN2 in asthma-COPD, COL15A1, GIMAP6, and JAM2 in asthma-IPF and LMO7, TSPAN13, LAMA3, and ANXA3 in COPD-IPF. Finally, analyzing drug-target networks suggested anti-inflammatory candidate drugs for treating the above mentioned diseases.

conclusionIn general, the results revealed the unique and common biomarkers among three chronic lung diseases. Eventually, some drugs were suggested for treatment purposes.

Indexed as

BiomarkersDisease SusceptibilityGene Expression RegulationGene Regulatory NetworksChronic DiseaseComputational BiologyDrug DiscoveryGene Expression ProfilingGene OntologyHumansLung DiseasesModels, TheoreticalMolecular Targeted TherapyTranscriptomeBiomarkersAsthmaBiomarkerChronic lung diseasesConsensusCOPDDrug-targetGene co-expression networkIPFModule

Identifiers

PMID31952466
PMCPMC6969427
OpenAlexW3005752665

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Registered trials

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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.