Evidence map›Paper›PMID 31419078›Full record

ArticleFEBS open bio2019

Identification of differentially expressed genes and signaling pathways in chronic obstructive pulmonary disease via bioinformatic analysis.

Xinwei Huang, Yunwei Li, Xiaoran Guo, Zongxin Zhu, Xiangyang Kong, Fubing Yu, Qiang Wang

Open access · goldAbstract read
In one paragraph

Article in FEBS open bio, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 27 citations in OpenAlex.

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  11. α-Arrestins and Their Functions: From Yeast to Human Health.International journal of molecular sciences · 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

7 authors at 3 institutions in 1 country.

Xinwei HuangFaculty of Environmental Science and Engineering, Kunming University of Science and Technology, China.
Yunwei LiMedical School, Kunming University of Science and Technology, China.
Xiaoran GuoMedical School, Kunming University of Science and Technology, China.
Zongxin ZhuMedical School, Kunming University of Science and Technology, China.
Xiangyang KongMedical School, Kunming University of Science and Technology, China.ORCID 0000-0001-8184-2493
Fubing YuDepartment of Gastroenterology, Fourth Affiliated Hospital of Kunming Medical University, China.
Qiang WangPhysical Examination Center, Second People's Hospital of Yunnan Province, Kunming, China.
Kunming University of Science and Technology · CNKunming Medical University · CNSecond People's Hospital of Yunnan Province · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD) is a multifactorial and heterogeneous disease that creates public health challenges worldwide. The underlying molecular mechanisms of COPD are not entirely clear. In this study, we aimed to identify the critical genes and potential molecular mechanisms of COPD by bioinformatic analysis. The gene expression profiles of lung tissues of COPD cases and healthy control subjects were obtained from the Gene Expression Omnibus. Differentially expressed genes were analyzed by integration with annotations from Gene Ontology and Kyoto Encyclopedia of Genes and Genomes, followed by construction of a protein-protein interaction network and weighted gene coexpression analysis. We identified 139 differentially expressed genes associated with the progression of COPD, among which 14 Hub genes were identified and found to be enriched in certain categories, including immune and inflammatory response, response to lipopolysaccharide and receptor for advanced glycation end products binding; in addition, these Hub genes are involved in multiple signaling pathways, particularly hematopoietic cell lineage and cytokine-cytokine receptor interaction. The 14 Hub genes were positively or negatively associated with COPD by wgcna analysis. The genes CX3CR1, PTGS2, FPR1, FPR2, S100A12, EGR1, CD163, S100A8 and S100A9 were identified to mediate inflammation and injury of the lung, and play critical roles in the pathogenesis of COPD. These findings improve our understanding of the underlying molecular mechanisms of COPD.

Indexed as

Computational BiologyDatabases, GeneticFemaleGene Expression RegulationGene Regulatory NetworksHumansMalePulmonary Disease, Chronic ObstructiveSignal Transductionbioinformatic analysischronic obstructive pulmonary diseasedifferentially expressed geneepidemiologyGEO data

Identifiers

PMID31419078
PMCPMC6823288
OpenAlexW2968241373

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.