Evidence map›Paper›PMID 32680596›Full record

ArticleAtherosclerosis2020

Genetic variations in G-protein signal pathways influence progression of coronary artery calcification: Results from the Heinz Nixdorf Recall study.

Stefanie Klenke, Nils Lehmann, Raimund Erbel, Karl-Heinz Jöckel, Winfried Siffert, Ulrich H Frey, Jürgen Peters

Abstract read
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In one paragraph

Article in Atherosclerosis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

7 citing papers in PubMed, 5 citations in OpenAlex.

  1. TheJournal of the American Heart Association · 2026
    Article
  2. Article
  3. Genetic variants of accessory proteins and G proteins in human genetic disease.Critical reviews in clinical laboratory sciences · 2025
    Review
  4. Review
  5. Single-Nucleotide Polymorphism in Genes Encoding G Protein SubunitsInternational journal of molecular sciences · 2023
    Article
  6. Article
  7. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Stefanie KlenkeKlinik für Anästhesiologie & Intensivmedizin, Universität Duisburg-Essen und Universitätsklinikum Essen, Essen, Germany. Electronic address: stefanie.klenke@uk-essen.de.
Nils LehmannInstitute for Medical Informatics, Biometry and Epidemiology, Universität Duisburg-Essen, Germany.
Raimund ErbelInstitute for Medical Informatics, Biometry and Epidemiology, Universität Duisburg-Essen, Germany.
Karl-Heinz JöckelInstitute for Medical Informatics, Biometry and Epidemiology, Universität Duisburg-Essen, Germany.
Winfried SiffertInstitut für Pharmakogenetik, Universität Duisburg-Essen and Universitätsklinikum Essen, Germany.
Ulrich H FreyKlinik für Anästhesiologie & Intensivmedizin, Universität Duisburg-Essen und Universitätsklinikum Essen, Essen, Germany; Klinik für Anästhesiologie, Operative Intensivmedizin, Schmerz- und Palliativmedizin, Marien Hospital Herne, Universitätsklinikum der Ruhr-Universität Bochum, Bochum, Germany.
Jürgen PetersKlinik für Anästhesiologie & Intensivmedizin, Universität Duisburg-Essen und Universitätsklinikum Essen, Essen, Germany.
Essen University Hospital · DEUniversity of Duisburg-Essen · DEUniversitätsklinikum Gießen und Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsCoronary artery calcification (CAC) is one of the most sensitive and specific markers of coronary atherosclerosis and believed to be heritable. We hypothesized that functionally relevant single-nucleotide polymorphisms (SNPs) in the G-protein signal pathway, which have been previously related to coronary artery disease, are associated with CAC progression.

methods3108 participants from the Heinz Nixdorf Recall study with CAC measurements at both baseline (CACb) and 5-year follow-up (CAC5y) were included. We genotyped SNPs rs1042714 (ADRB2), rs6026584 and rs12481583 (GNAS), and rs5443 (GNB3) and defined a priori risk alleles derived from literature data. Regression analyses were applied to measures of 5-year CAC progression, unadjusted, adjusted for age, sex, and adjusted for age, sex, log(CACb+1) as well as for cardiovascular risk factors.

resultsThe presence of one or more risk alleles was associated with a 26.9% (95% CI 5.5-52.4) increase in 5-year CAC progression (p = 0.011) and a 29.2% (95% CI 5.9-57.6) accelerated increase of CAC over the 5-year period compared to what was expected with respect to the baseline CAC percentile value (p = 0.012). Each of those risk alleles increased the 5-year CAC progression by 4.4% (95% CI 1.3-7.6, p = 0.006) and resulted in a 4.9% accelerated increase of CAC over the 5-year period (95% CI 1.6-8.4, p = 0.004). These unadjusted data did not change after adjustment.

conclusionsGenetic variations in the G-protein signal pathway are associated with CAC progression in a cumulative fashion, indicating the importance of the pathway for genetic heritability in CAC progression and coronary artery disease.

Indexed as

Coronary Artery DiseaseVascular CalcificationDisease ProgressionGTP-Binding ProteinsHumansPolymorphism, Single NucleotideRisk FactorsSignal TransductionGTP-Binding ProteinsCAC ProgressionCoronary artery diseaseGeneticG-proteinSNPs

Identifiers

PMID32680596
OpenAlexW3039612117

What OpenQuestion holds

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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.