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pmid:34922439

Identifying the hub genes for Duchenne muscular dystrophy and Becker muscular dystrophy by weighted correlation network analysis.

Junjie Wang · Qin Fan · Tengbo Yu · Yingze Zhang

BMC genomic data · 2021 doi:10.1186/s12863-021-01014-w

Paper

complete

Experiment

complete

Data

partial

Analysis

partial

Execution

absent

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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title
Identifying the hub genes for Duchenne muscular dystrophy and Becker muscular dystrophy by weighted correlation network analysis.
doi
10.1186/s12863-021-01014-w
pmid
34922439
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[0]
Junjie Wang
[1]
Qin Fan
[2]
Tengbo Yu
[3]
Yingze Zhang
journal
BMC genomic data
year
2021
abstract
BACKGROUND: The goal of this study is to identify the hub genes for Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) via weighted correlation network analysis (WGCNA). METHODS: The gene expression profile of vastus lateralis biopsy samples obtained in 17 patients with DMD, 11 patients with BMD and 6 healthy individuals was downloaded from the Gene Expression Omnibus (GEO) database (GSE109178). After obtaining different expressed genes (DEGs) via GEO2R, WGCNA was conducted using R package, modules and genes that highly associated with DMD, BMD, and their age or pathology were screened. Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analysis and protein-protein interaction (PPI) network analysis were also conducted. Hub genes and highly correlated clustered genes were identified using Search Tool for the Retrieval of Interacting Genes (STRING) and Cystoscape software. RESULTS: One thousand four hundred seventy DEGs were identified between DMD and control, with 1281 upregulated and 189 downregulated DEGs. Four hundred and twenty DEGs were found between BMD and control, with 157 upregulated and 263 upregulated DEGs. Fourteen modules with different colors were identified for DMD vs control, and 7 modules with different colors were identified for BMD vs control. Ten hub genes were summarized for DMD and BMD respectively, 5 hub genes were summarized for BMD age, 5 and 3 highly correlated clustered genes were summarized for DMD age and BMD pathology, respectively. In addition, 20 GO enrichments were found to be involved in DMD, 3 GO enrichments were found to be involved in BMD, 3 GO enrichments were found to be involved in BMD age. CONCLUSION: In DMD, several hub genes were identified: C3AR1, TLR7, IRF8, FYB and CD33(immune and inflammation associated genes), TYROBP, PLEK, AIF1(actin reorganization associated genes), LAPTM5 and NT5E(cell death and arterial calcification associated genes, respectively). In BMD, a number of hub genes were identified: LOX, ELN, PLEK, IKZF1, CTSK, THBS2, ADAMTS2, COL5A1(extracellular matrix associated genes), BCL2L1 and CDK2(cell cycle associated genes).
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After obtaining DEGs via GEO2R, WGCNA was conducted using an R package.
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As a bioinformatics analysis, there are no patient data sets.
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Weighted correlation network analysis identified ten hub genes each for Duchenne muscular dystrophy and Becker muscular dystrophy.
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Ten hub genes were summarized for DMD and BMD respectively, 5 hub genes were summarized for BMD age, 5 and 3 highly correlated clustered genes were summarized for DMD age and BMD pathology, respectively.
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Weighted correlation network analysis identified ten hub genes each for Duchenne muscular dystrophy and Becker muscular dystrophy.
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title
Asynchronous remodeling is a driver of failed regeneration in Duchenne muscular dystrophy
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:34922439", "kind": "science-record", "revision": 4, "content_hash": "sha256:07cf8eea9c07e806ac7aa62ac9a044272d0d222a29eb47cef1216baca606de54", "created_at": "2026-11-01T17:36:38Z", "updated_at": "2026-11-01T22:05:23Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Identifying the hub genes for Duchenne muscular dystrophy and Becker muscular dystrophy by weighted correlation network analysis.", "doi": "10.1186/s12863-021-01014-w", "pmid": "34922439", "authors": ["Junjie Wang", "Qin Fan", "Tengbo Yu", "Yingze Zhang"], "journal": "BMC genomic data", "year": 2021, "abstract": "BACKGROUND: The goal of this study is to identify the hub genes for Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD) via weighted correlation network analysis (WGCNA).\nMETHODS: The gene expression profile of vastus lateralis biopsy samples obtained in 17 patients with DMD, 11 patients with BMD and 6 healthy individuals was downloaded from the Gene Expression Omnibus (GEO) database (GSE109178). After obtaining different expressed genes (DEGs) via GEO2R, WGCNA was conducted using R package, modules and genes that highly associated with DMD, BMD, and their age or pathology were screened. Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment analysis and protein-protein interaction (PPI) network analysis were also conducted. Hub genes and highly correlated clustered genes were identified using Search Tool for the Retrieval of Interacting Genes (STRING) and Cystoscape software.\nRESULTS: One thousand four hundred seventy DEGs were identified between DMD and control, with 1281 upregulated and 189 downregulated DEGs. Four hundred and twenty DEGs were found between BMD and control, with 157 upregulated and 263 upregulated DEGs. Fourteen modules with different colors were identified for DMD vs control, and 7 modules with different colors were identified for BMD vs control. Ten hub genes were summarized for DMD and BMD respectively, 5 hub genes were summarized for BMD age, 5 and 3 highly correlated clustered genes were summarized for DMD age and BMD pathology, respectively. In addition, 20 GO enrichments were found to be involved in DMD, 3 GO enrichments were found to be involved in BMD, 3 GO enrichments were found to be involved in BMD age.\nCONCLUSION: In DMD, several hub genes were identified: C3AR1, TLR7, IRF8, FYB and CD33(immune and inflammation associated genes), TYROBP, PLEK, AIF1(actin reorganization associated genes), LAPTM5 and NT5E(cell death and arterial calcification associated genes, respectively). 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