Evidence map›Paper›PMID 34271875›Full record

ArticleBMC cardiovascular disorders2021

KLRD1, FOSL2 and LILRB3 as potential biomarkers for plaques progression in acute myocardial infarction and stable coronary artery disease.

Qiang Zhang, Yue Zheng, Meng Ning, Tong Li

Open access · goldAbstract read
In one paragraph

Article in BMC cardiovascular disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  6. Exploring the underlying molecular mechanisms of acute myocardial infarction after SARS-CoV-2 infection.American heart journal plus : cardiology research and practice · 2024
    Article
  7. Progress in the Study of Fra-2 in Respiratory Diseases.International journal of molecular sciences · 2024
    Review
  8. Article
  9. 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

4 authors at 1 institution in 2 countries.

Qiang Zhang *Cardiology, The Third Central Clinical College of Tianjin Medical University, No. 83, Jintang Road, Hedong District, Tianjin, 300170, China.
Yue Zheng *Cardiology, The Third Central Clinical College of Tianjin Medical University, No. 83, Jintang Road, Hedong District, Tianjin, 300170, China.
Meng Ning *Cardiology, The Third Central Clinical College of Tianjin Medical University, No. 83, Jintang Road, Hedong District, Tianjin, 300170, China.
Tong LiCardiology, The Third Central Clinical College of Tianjin Medical University, No. 83, Jintang Road, Hedong District, Tianjin, 300170, China. litong3zx@sina.com.ORCID 0000-0002-6281-5163
Nankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial infarction (MI) contributes to high mortality and morbidity and can also accelerate atherosclerosis, thus inducing recurrent event due to status changing of coronary artery walls or plaques. The research aimed to investigate the differentially expressed genes (DEGs), which may be potential therapeutic targets for plaques progression in stable coronary artery disease (CAD) and ST-elevated MI (STEMI).

methodsTwo human datasets (GSE56885 and GSE59867) were analyzed by GEO2R and enrichment analysis was applied through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. To explore the seed genes, the protein-protein interaction (PPI) network was constructed and seed genes, as well as top30 ranking neighbours were screened out. To validate these findings, one human dataset GSE120521 was analyzed. Linear regression analysis and ROC curve were also performed to determine which seed genes above mentioned could be independent factors for plaques progression. Mice MI model and ELISA of seed genes were applied and ROC curve was also performed for in vivo validation.

results169 DEGs and 573 DEGs were screened out in GSE56885 and GSE59867, respectively. Utilizing GO and KEGG analysis, these DEGs mainly enriched in immune system response and cytokines interaction. PPI network analysis was carried out and 19 seed genes were screened out. To validate these findings, GSE120521 was analyzed and three genes were demonstrated to be targets for plaques progression and stable CAD progression, including KLRD1, FOSL2 and LILRB3. KLRD1 and LILRB3 were demonstrated to be high-expressed at 1d after MI compared to SHAM group and FOSL2 expression was low-expressed at 1d and 1w. To investigate the diagnostic abilities of seed genes, ROC analysis was applied and the AUCs of KLRD1, FOSL2 and LILRB3, were 0.771, 0.938 and 0.972, respectively.

conclusionThis study provided the screened seed genes, KLRD1, FOSL2 and LILRB3, as credible molecular biomarkers for plaques status changing in CAD progression and MI recurrence. Other seed genes, such as FOS, SOCS3 and MCL1, may also be potential targets for treatment due to their special clinical value in cardiovascular diseases.

Indexed as

Plaque, AtheroscleroticAnimalsAntigens, CDCase-Control StudiesCoronary Artery DiseaseDatabases, GeneticDisease Models, AnimalDisease ProgressionFos-Related Antigen-2Gene Regulatory NetworksGenetic MarkersHumansMaleMiceMice, Inbred C57BLNK Cell Lectin-Like Receptor Subfamily DAntigens, CDFOSL2 protein, humanFosl2 protein, mouseFos-Related Antigen-2Genetic MarkersKLRD1 protein, humanKlrd1 protein, mouseLILRB3 protein, humanNK Cell Lectin-Like Receptor Subfamily DPirb protein, mouseReceptors, ImmunologicGEOPPIStable CADSTEMIWebGestalt

Identifiers

PMID34271875
PMCPMC8285847
OpenAlexW3178435834

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.