Evidence map›Paper›PMID 32373157›Full record

ArticleFrontiers in genetics2020

The Integrated Landscape of Biological Candidate Causal Genes in Coronary Artery Disease.

Qiwen Zheng, Yujia Ma, Si Chen, Qianzi Che, Dafang Chen

Open access · goldAbstract read
In one paragraph

Article in Frontiers in genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Collagen IV in Gould syndrome and Alport syndrome.Nature reviews. Nephrology · 2025
    Review
  2. Article
  3. Article
  4. The Study of the Association of Polymorphisms inInternational journal of molecular sciences · 2023
    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

5 authors at 1 institution in 1 country.

Qiwen ZhengDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.
Yujia MaDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.
Si ChenDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.
Qianzi CheDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.
Dafang ChenDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenome-wide association studies (GWASs) have identified more than 150 genetic loci that demonstrate robust association with coronary artery disease (CAD). In contrast to the success of GWAS, the translation from statistical signals to biological mechanism and exploration of causal genes for drug development remain difficult, owing to the complexity of gene regulatory and linkage disequilibrium patterns. We aim to prioritize the plausible causal genes for CAD at a genome-wide level.

methodsWe integrated the latest GWAS summary statistics with other omics data from different layers and utilized eight different computational methods to predict CAD potential causal genes. The prioritized candidate genes were further characterized by pathway enrichment analysis, tissue-specific expression analysis, and pathway crosstalk analysis.

resultsOur analysis identified 55 high-confidence causal genes for CAD, among which 15 genes (

conclusionOur study delineated the landscape of CAD potential causal genes and highlighted several biological processes involved in CAD pathogenesis. Further studies and experimental validations of these genes may shed light on mechanistic insights into CAD development and provide potential drug targets for future therapeutics.

Indexed as

causal genescoronary artery diseaseexpression quantitative trait locusgenome-wide association studiesintegration analysisnetworkprioritizeprotein–protein interaction

Identifiers

PMID32373157
PMCPMC7186505
OpenAlexW3020734836

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.