Evidence map›Paper›PMID 30643084›Full record

ArticleJournal of atherosclerosis and thrombosis2019

Investigation of the Underlying Genes and Mechanism of Macrophage-Enriched Ruptured Atherosclerotic Plaques Using Bioinformatics Method.

Hao Wang, Dongyuan Liu, Hongbing Zhang

Open access · diamondAbstract read
In one paragraph

Article in Journal of atherosclerosis and thrombosis, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-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

17 citing papers in PubMed, 33 citations in OpenAlex.

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  8. Frontiers in immunology · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Macrophage Plasticity and Atherosclerosis Therapy.Frontiers in molecular biosciences · 2021
    Review
  13. Genetic landscape and autoimmunity of monocytes in developing Vogt-Koyanagi-Harada disease.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  14. Article
  15. 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

3 authors at 1 institution in 1 country.

Hao WangDepartment of Neurosurgery, Beijing Luhe Hospital, Capital Medical University.
Dongyuan LiuDepartment of Neurosurgery, Beijing Luhe Hospital, Capital Medical University.
Hongbing ZhangDepartment of Neurosurgery, Beijing Luhe Hospital, Capital Medical University.
Beijing Luhe Hospital Affiliated to Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimThe study aimed to identify the underlying differentially expressed genes (DEGs) and mechanism of macrophage-enriched rupture atherosclerotic plaque using bioinformatics methods.

methodsGSE41571, which includes six stable samples and five ruptured atherosclerotic samples, was downloaded from the GEO database. After preprocessing, DEGs between ruptured and stable atherosclerotic samples were identified using LIMMA. Gene Ontology biological process (GO_BP) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs were performed using the Database for Annotation, Visualization, and Integration Discovery (DAVID) online tool. Based on the STRING database, protein-protein interactions (PPIs) network among DEGs were constructed. Regulatory relationships between miRNAs/transcriptional factors (TFs) and target genes were predicted using Enrichr, and regulatory networks were visualized using Cytoscape.

resultsA total of 268 DEGs (64 up-regulated and 204 down-regulated DEGs) were identified between ruptured and stable samples. In the PPI network, collagen type III alpha 1 chain (COL3A1), collagen type I alpha 2 chain (COL1A2), and asporin (ASPN) were more than 15 interaction degrees. In the miRNA-target network, miR21 was highlighted with highest degrees and ASPN could be targeted by miR21. Functional enrichment analysis showed that COL3A1 and COL1A2 were significantly enriched in extracellular matrix organization and cell adhesion GO_BP terms. Pre-platelet basic protein (PPBP) was the most significantly up-regulated gene in ruptured atherosclerotic samples and enriched in immune response and inflammatory response GO_BP terms.

conclusionsDown-regulated COL3A1, COL1A2 and ASPN, and up-regulated PPBP might perform critical promotional roles in atherosclerotic plaque rupture. Furthermore, miR21 might be potential target to prevent atherosclerotic rupture.

Indexed as

Gene Expression ProfilingTranscriptomebeta-ThromboglobulinCollagen Type ICollagen Type IIIComputational BiologyDown-RegulationExtracellular Matrix ProteinsGene OntologyHumansMacrophagesMicroRNAsPlaque, AtheroscleroticProtein Interaction MappingTranscription FactorsUp-RegulationASPN protein, humanbeta-ThromboglobulinCOL1A2 protein, humanCOL3A1 protein, humanCollagen Type ICollagen Type IIIExtracellular Matrix ProteinsMicroRNAsMIRN21 microRNA, humanPPBP protein, humanTranscription FactorsAtherosclerosisDifferentially Expressed GenesMacrophagesmicroRNARuptured atherosclerotic plaqueTranscription factors

Identifiers

PMID30643084
PMCPMC6629752
OpenAlexW2911162611

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.