Evidence map›Paper›PMID 32594047›Full record

ArticleNeural regeneration research2020

Hub genes and key pathways of traumatic brain injury: bioinformatics analysis and

Yun-Liang Tang, Long-Jun Fang, Ling-Yang Zhong, Jian Jiang, Xiao-Yang Dong, Zhen Feng

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 13% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Pooled it
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  16. Potential Progression Mechanism and Key Genes in Early Stage of mTBI.Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
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  18. Comparative transcriptomic analysis of ratNeural regeneration research · 2021
    Article
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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

6 authors at 2 institutions in 1 country.

Yun-Liang TangDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Long-Jun FangDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Ling-Yang ZhongDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Jian JiangDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Xiao-Yang DongDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Zhen FengDepartment of Rehabilitation Medicine, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi Province, China.
Nanchang University · CNFirst Affiliated Hospital of Nanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The exact mechanisms associated with secondary brain damage following traumatic brain injury (TBI) remain unclear; therefore, identifying the critical molecular mechanisms involved in TBI is essential. The mRNA expression microarray GSE2871 was downloaded from the Gene Expression Omnibus (GEO) repository. GSE2871 comprises a total of 31 cerebral cortex samples, including two post-TBI time points. The microarray features eight control and seven TBI samples, from 4 hours post-TBI, and eight control and eight TBI samples from 24 hours post-TBI. In this bioinformatics-based study, 109 and 66 differentially expressed genes (DEGs) were identified in a Sprague-Dawley (SD) rat TBI model, 4 and 24 hours post-TBI, respectively. Functional enrichment analysis showed that the identified DEGs were significantly enriched in several terms, such as positive regulation of nuclear factor-κB transcription factor activity, mitogen-activated protein kinase signaling pathway, negative regulation of apoptotic process, and tumor necrosis factor signaling pathway. Moreover, the hub genes with high connectivity degrees were primarily related to inflammatory mediators. To validate the top five hub genes, a rat model of TBI was established using the weight-drop method, and real-time quantitative polymerase chain reaction analysis of the cerebral cortex was performed. The results showed that compared with control rats, Tnf-α, c-Myc, Spp1, Cxcl10, Ptprc, Egf, Mmp9, and Lcn2 were upregulated, and Fn1 was downregulated in TBI rats. Among these hub genes, Fn1, c-Myc, and Ptprc may represent novel biomarkers or therapeutic targets for TBI. These identified pathways and key genes may provide insights into the molecular mechanisms of TBI and provide potential treatment targets for patients with TBI. This study was approved by the Experimental Animal Ethics Committee of the First Affiliated Hospital of Nanchang University, China (approval No. 003) in January 2016.

Indexed as

bioinformaticsDEGsdifferentially expressed genesGene Ontologyhub genesinflammationKyoto Encyclopedia of Genes and Genomesmolecular mechanismtraumatic brain injury

Identifiers

PMID32594047
PMCPMC7749465
OpenAlexW3036334742

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.