Evidence map›Paper›PMID 33987395›Full record

ArticleAnnals of translational medicine2021

Transcriptome sequencing and analysis reveals the molecular mechanism of skeletal muscle atrophy induced by denervation.

Xin Chen, Ming Li, Bairong Chen, Wei Wang, Lilei Zhang, Yanan Ji, Zehao Chen, Xuejun Ni, Yuntian Shen, Hualin Sun

Open access · diamondAbstract read
In one paragraph

Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

  1. Muscle fibre denervation in ageing.Clinical science (London, England : 1979) · 2026
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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

10 authors at 2 institutions in 1 country.

Xin ChenDepartment of Neurology, Affiliated Hospital of Nantong University, Nantong, China.
Ming LiDepartment of Laboratory, People's Hospital of Binhai County, Yancheng, China.
Bairong ChenDepartment of Medical Laboratory, School of Public Health, Nantong University, Nantong, China.
Wei WangKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Lilei ZhangKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Yanan JiKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Zehao ChenKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Xuejun NiDepartment of Ultrasound, Affiliated Hospital of Nantong University, Nantong, China.
Yuntian ShenKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Hualin SunKey Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Jiangsu Clinical Medicine Center of Tissue Engineering and Nerve Injury Repair, Co-Innovation Center of Neuroregeneration, Nantong University, Nantong, China.
Nantong University · CNBinzhou People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe molecular mechanism of denervated muscle atrophy is very complex and has not been elucidated to date. In this study, we aimed to use transcriptome sequencing technology to systematically analyze the molecular mechanism of denervated muscle atrophy in order to eventually develop effective strategies or drugs to prevent muscle atrophy.

methodsTranscriptome sequencing technology was used to analyze the differentially expressed genes (DEGs) in denervated skeletal muscles. Unsupervised hierarchical clustering of DEGs was performed. Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was used to analyze the DEGs.

resultsResults showed that 2,749 transcripts were up-regulated, and 2,941 transcripts were down-regulated in denervated tibialis anterior (TA) muscles after 14 days of denervation. The up-regulated expressed genes were analyzed through GO and the results demonstrated that biological processes of the up-regulated expressed genes included apoptotic process, cellular response to DNA damage stimulus, aging, and protein ubiquitination; the cellular component of the up-regulated expressed genes included cytoplasm, cytoskeleton, and nucleus; and the molecular function of the up-regulated expressed genes included ubiquitin-protein transferase activity and hydrolase activity. The KEGG pathway of the up-regulated expressed genes included ubiquitin mediated proteolysis, Fc gamma R-mediated phagocytosis, and transforming growth factor-beta (TGF-β) signaling pathway. The biological processes of the down-regulated expressed genes included angiogenesis, tricarboxylic acid cycle, adenosine triphosphate (ATP) biosynthetic process, muscle contraction, gluconeogenesis; the cellular component of the down-regulated expressed genes included mitochondrion, cytoskeleton, and myofibril; and the molecular function of the down-regulated expressed genes included nicotinamide adenine dinucleotide plus hydrogen (NADH) dehydrogenase (ubiquinone) activity, proton-transporting ATP synthase activity, ATP binding, electron carrier activity, cytochrome-c oxidase activity, and oxidoreductase activity. The KEGG pathway of the down-regulated expressed genes included oxidative phosphorylation, tricarboxylic acid cycle, glycolysis/gluconeogenesis, and the PI3K-Akt signaling pathway.

conclusionsA huge number of DEGs were identified in TA muscles after denervation. The up-regulated expressed genes mainly involve in proteolysis, apoptosis, and ageing. The down-regulated expressed genes mainly involve in energy metabolism, angiogenesis, and protein synthesis. This study further enriched the molecular mechanism of denervation-induced muscle atrophy.

Indexed as

energy metabolismmuscle atrophyPeripheral nerve injuryproteolysistranscriptome sequencing

Identifiers

PMID33987395
PMCPMC8106053
OpenAlexW3157687069

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.