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pmid:35990248

Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress.

Guoqi Zhu · Yan Lai · Fei Chen · Jun Qian · Hao Lin · Deqiang Yuan · Tongqing Yao · XueBo Liu

Disease markers · 2022 doi:10.1155/2022/6306845

Paper

complete

Experiment

complete

Data

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Analysis

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Execution

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Record details sci_version · id · kind · revision · content_hash · schema · created_at · updated_at · generator
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pmid:35990248
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2026-11-01T18:15:07Z
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2026-11-01T22:49:50Z
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paper object · 10 fields
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title
Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress.
doi
10.1155/2022/6306845
pmid
35990248
authors array · 8 items
[0]
Guoqi Zhu
[1]
Yan Lai
[2]
Fei Chen
[3]
Jun Qian
[4]
Hao Lin
[5]
Deqiang Yuan
[6]
Tongqing Yao
[7]
XueBo Liu
journal
Disease markers
year
2022
abstract
Background: Abnormal endothelial shear stress (ESS) is a significant risk factor for atherosclerosis (AS); however, the genes and pathways between ESS and AS are poorly understood. Here, we screened hub genes and potential regulatory targets linked to the progression of AS induced by abnormal ESS. Methods: The microarray data of ESS and AS were downloaded from the Gene Expression Omnibus (GEO) database. The coexpression modules related to shear stress and AS were identified with weighted gene coexpression network analysis (WGCNA). Coexpression genes in modules obtained from GSE28829 and GSE160611 were considered as SET1. The results were validated in validation set by differential gene analysis. The limma package in R was used to identify differentially expressed genes (DEGs). The common DEGs of GSE100927 and GSE103672 were regarded as SET2. Next, Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted. Protein-protein interaction (PPI) enrichment analysis was assembled, and hub genes were identified using MCODE and ClueGO in Cytoscape. ROC curve analyses were conducted to assess the ability of common hub genes to distinguish samples of atherosclerotic plaque from normal arterial. The expression of common hub gene was verified in ox-LDL-induced foam cells and GSE41571. Results: We identified three gene modules (the blue, tan, and cyan modules) related to AS and three shear stress-related modules (the brown, red, and pink modules). A total of 129 genes in SET1 and 476 genes in SET2 were identified. CCRL2, LGALS9, and PLCB2 were identified as common hub genes and validated in the GSE100927, GSE28829, and GSE41571. ROC analysis indicates the expression of CCRL2, LGALS9, and PLCB2 could effectively distinguish the atherosclerotic plaque and normal arterial. The expression level of CCRL2, LGALS9, and PLCB2 increases with the accumulation of lipid increased. Conclusion: We identified CCRL2, LGALS9, and PLCB2 as key genes associated with abnormal ESS and AS and may provide potential prevention and treatment target of AS induced by abnormal ESS.
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Differential gene expression was performed with limma package with |log FC| > 0.5 and adjusted P value < 0.05 [23].
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sections[5] "2.3. Validation of Gene Expression through DEG Analysis" paragraph 2
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Differential gene expression was performed with limma package with |log FC| > 0.5 and adjusted P value < 0.05 [23].
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sections[24] "Data Availability" paragraph 2
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Datasets used in this study were obtained from open public databases (https://www.ncbi.nlm.nih.gov/geo/), but the datasets analyzed in this study are available from the corresponding authors on request.
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CCRL2, LGALS9, and PLCB2 were identified as common hub genes associated with abnormal endothelial shear stress and atherosclerosis.
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We identified CCRL2, LGALS9, and PLCB2 as key genes associated with abnormal ESS and AS and may provide potential prevention and treatment target of AS induced by abnormal ESS.
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CCRL2, LGALS9, and PLCB2 were identified as common hub genes associated with abnormal endothelial shear stress and atherosclerosis.
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Atherosclerotic and control peripheral artery gene expression
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Longitudinal Transcriptional Response of Endothelial Cells to Shear Stress
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The paper names the method it used and the corpus's method extractor maps it onto the DSL catalogue: limma_voom.
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GSE160611
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GSE103672
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GSE100927
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GSE28829
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GSE41571
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GSE160611
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GSE103672
[2]
GSE100927
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GSE28829
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GSE41571
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Datasets used in this study were obtained from open public databases (https://www.ncbi.nlm.nih.gov/geo/), but the datasets analyzed in this study are available from the corresponding authors on request.
basis
The paper names GSE160611, GSE103672, GSE100927, GSE28829, GSE41571 in Gene Expression Omnibus (GEO) and the accession resolves in the repository. No dataset was downloaded and no licence was read.
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fdr_bh
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PMID 35990248 full text
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of AS induced by abnormal ESS. Methods: The microarray data of ESS and AS were downloaded from the
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Differential gene expression was performed with limma package with |log FC| > 0.5 and adjusted P value < 0.05 [23].
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Complete file
{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:35990248", "kind": "science-record", "revision": 5, "content_hash": "sha256:eb783bf59046a148cbd92a641f0b2afcc67a7929bd6219b051c3023cc2c90b8d", "created_at": "2026-11-01T18:15:07Z", "updated_at": "2026-11-01T22:49:50Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "Exploration of the Crucial Genes and Molecular Mechanisms Mediating Atherosclerosis and Abnormal Endothelial Shear Stress.", "doi": "10.1155/2022/6306845", "pmid": "35990248", "authors": ["Guoqi Zhu", "Yan Lai", "Fei Chen", "Jun Qian", "Hao Lin", "Deqiang Yuan", "Tongqing Yao", "XueBo Liu"], "journal": "Disease markers", "year": 2022, "abstract": "Background: Abnormal endothelial shear stress (ESS) is a significant risk factor for atherosclerosis (AS); however, the genes and pathways between ESS and AS are poorly understood. Here, we screened hub genes and potential regulatory targets linked to the progression of AS induced by abnormal ESS.\nMethods: The microarray data of ESS and AS were downloaded from the Gene Expression Omnibus (GEO) database. The coexpression modules related to shear stress and AS were identified with weighted gene coexpression network analysis (WGCNA). Coexpression genes in modules obtained from GSE28829 and GSE160611 were considered as SET1. The results were validated in validation set by differential gene analysis. The limma package in R was used to identify differentially expressed genes (DEGs). The common DEGs of GSE100927 and GSE103672 were regarded as SET2. Next, Gene Ontology (GO) annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis was conducted. Protein-protein interaction (PPI) enrichment analysis was assembled, and hub genes were identified using MCODE and ClueGO in Cytoscape. ROC curve analyses were conducted to assess the ability of common hub genes to distinguish samples of atherosclerotic plaque from normal arterial. The expression of common hub gene was verified in ox-LDL-induced foam cells and GSE41571.\nResults: We identified three gene modules (the blue, tan, and cyan modules) related to AS and three shear stress-related modules (the brown, red, and pink modules). A total of 129 genes in SET1 and 476 genes in SET2 were identified. CCRL2, LGALS9, and PLCB2 were identified as common hub genes and validated in the GSE100927, GSE28829, and GSE41571. ROC analysis indicates the expression of CCRL2, LGALS9, and PLCB2 could effectively distinguish the atherosclerotic plaque and normal arterial. The expression level of CCRL2, LGALS9, and PLCB2 increases with the accumulation of lipid increased.\nConclusion: We identified CCRL2, LGALS9, and PLCB2 as key genes associated with abnormal ESS and AS and may provide potential prevention and treatment target of AS induced by abnormal ESS.", "claims": [{"id": "claim-method", "statement": "Differential gene expression was performed with limma package with |log FC| > 0.5 and adjusted P value < 0.05 [23].", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:35990248", "locator": "sections[5] \"2.3. Validation of Gene Expression through DEG Analysis\" paragraph 2", "quote": "Differential gene expression was performed with limma package with |log FC| > 0.5 and adjusted P value < 0.05 [23]."}], "state": "complete"}, {"id": "claim-data-access", "statement": "Datasets used in this study were obtained from open public databases (https://www.ncbi.nlm.nih.gov/geo/), but the datasets analyzed in this study are available from the corresponding authors on request.", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:35990248", "locator": "sections[24] \"Data Availability\" paragraph 2", "quote": "Datasets used in this study were obtained from open public databases (https://www.ncbi.nlm.nih.gov/geo/), but the datasets analyzed in this study are available from the corresponding authors on request."}], "state": "complete"}, {"id": "claim-target-result", "statement": "CCRL2, LGALS9, and PLCB2 were identified as common hub genes associated with abnormal endothelial shear stress and atherosclerosis.", "kind": "qualitative", "target": null, "evidence": [{"asset": "source:pmid:35990248", "locator": "sections[0] \"Abstract\" paragraph 4", "quote": "We identified CCRL2, LGALS9, and PLCB2 as key genes associated with abnormal ESS and AS and may provide potential prevention and treatment target of AS induced by abnormal ESS."}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "CCRL2, LGALS9, and PLCB2 were identified as common hub genes associated with abnormal endothelial shear stress and atherosclerosis.", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:35990248"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. This lane did not download the dataset or read its licence.", "duration_hours": null, "parameters": {}, "inputs": ["data:geo:GSE100927"], "outputs": ["the source data with its repository provenance"], "instruments": [], "reagents": []}, {"id": "run_analysis", "order": 3, "name": "Run the published analysis", "kind": "analysis", "state": "complete", "blocked_on": null, "description": "Apply the paper's statistical method to the resolved series and compare the result with the published target.", "duration_hours": null, "parameters": {}, "inputs": ["data:geo:GSE100927"], "outputs": ["the replicated result and its comparison"], "instruments": [], "reagents": []}], "materials": [], "instruments": [], "reagents": [], "conditions": {}, "gaps": []}, "data": {"state": "partial", "assets": [{"id": "source:pmid:35990248", "role": "manuscript", "format": "xml", "media_type": "application/xml", "uri": "https://doi.org/10.1155/2022/6306845", "sha256": 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The physical bench the paper used is not, so a physical validation cannot be run here."}, "data": {"tier": "R1", "reachable": true, "accessions": ["GSE160611", "GSE103672", "GSE100927", "GSE28829", "GSE41571"], "resolved_accessions": ["GSE160611", "GSE103672", "GSE100927", "GSE28829", "GSE41571"], "statements": ["Datasets used in this study were obtained from open public databases (https://www.ncbi.nlm.nih.gov/geo/), but the datasets analyzed in this study are available from the corresponding authors on request."], "basis": "The paper names GSE160611, GSE103672, GSE100927, GSE28829, GSE41571 in Gene Expression Omnibus (GEO) and the accession resolves in the repository. 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