Evidence map›Paper›PMID 33672678›Full record

ArticleMolecules (Basel, Switzerland)2021

Identification of Key Candidate Genes Involved in the Progression of Idiopathic Pulmonary Fibrosis.

Yu Cui, Jie Ji, Jiwei Hou, Yi Tan, Xiaodong Han

Abstract read
In one paragraph

Article in Molecules (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

17 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  11. An explainable machine learning-driven proposal of pulmonary fibrosis biomarkers.Computational and structural biotechnology journal · 2023
    Article
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  13. Mechanism of action ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 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

5 authors.

Yu CuiImmunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.ORCID 0000-0002-2113-6105
Jie JiImmunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.
Jiwei HouImmunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.
Yi TanImmunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.
Xiaodong HanImmunology and Reproduction Biology Laboratory & State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Hankou Road 22, Nanjing 210093, China.

Funding

National Natural Science Foundation of China 81570059, 31370524the Natural Science Foundation of Jiangsu Province of China BK20151398
6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a lethal, agnogenic interstitial lung disease with limited therapeutic options. To investigate vital genes involved in the development of IPF, we integrated and compared four expression profiles (GSE110147, GSE53845, GSE24206, and GSE10667), including 87 IPF samples and 40 normal samples. By reanalyzing these datasets, we managed to identify 62 upregulated genes and 20 downregulated genes in IPF samples compared with normal samples. Differentially expressed genes (DEGs) were analyzed by gene ontology and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis to illustrate relevant pathways of IPF, biological processes, molecular function, and cell components. The DEGs were then subjected to protein-protein interaction (PPI) for network analysis, serving to find 11 key candidate genes (ANXA3, STX11, THBS2, MMP1, MMP9, MMP7, MMP10, SPP1, COL1A1, ITGB8, IGF1). The result of RT-qPCR and immunohistochemical staining verified our finding as well. In summary, we identified 11 key candidate genes related to the process of IPF, which may contribute to novel treatments of IPF.

Indexed as

Annexin A3Collagen Type ICollagen Type I, alpha 1 ChainDatabases, GeneticGene Expression ProfilingGene OntologyHumansIdiopathic Pulmonary FibrosisInsulin-Like Growth Factor IIntegrin beta ChainsMatrix MetalloproteinasesOsteopontinProtein Interaction MapsQa-SNARE ProteinsThrombospondin 2ThrombospondinsAnnexin A3ANXA3 protein, humanCollagen Type ICollagen Type I, alpha 1 ChainIGF1 protein, humanInsulin-Like Growth Factor IIntegrin beta ChainsITGB8 protein, humanMatrix MetalloproteinasesOsteopontinQa-SNARE ProteinsSPP1 protein, humanSTX11 protein, humanThrombospondin 2ThrombospondinsIGF-1intergrinIPFMMPOPN

Identifiers

PMID33672678
PMCPMC7924352

What OpenQuestion holds

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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.