ArticleCurrent genetic medicine reports2018
Genetics of Subclinical Coronary Atherosclerosis.
Article in Current genetic medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Molecular profiling of coronary stent testenosis: A systematic review and functional analysis of implicated genes.Medicine · 2026Pooled it
- Type 2 Diabetes Modifies the Association of CAD Genomic Risk Variants With Subclinical Atherosclerosis.Circulation. Genomic and precision medicine · 2023Article
- Epigenetics of single-site and multi-site atherosclerosis in African Americans from the Genetic Epidemiology Network of Arteriopathy (GENOA).Clinical epigenetics · 2022Article
- Apolipoprotein E and Atherosclerosis.Current atherosclerosis reports · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
purpose of reviewThis review highlights recent findings regarding genetics of coronary artery calcification (CAC), a marker of subclinical atherosclerosis burden, that is a precursor of clinical coronary artery disease. RECENT
findingsCAC quantity is heritable. Genome wide association studies of common single nucleotide polymorphisms have identified genomic regions explaining ~2.4% of CAC heritability. Low frequency and rare variants explain additional variation in CAC. Evidence suggests that there may be different genetic etiologies for variation in CAC progression than for cross-sectional measures of CAC. Studies integrating multiple -omics data are providing new insights into the pathobiology of subclinical coronary atherosclerosis. SUMMARY: The future is promising for innovative studies utilizing whole genome sequencing data as well as other -omics such as epigenomic modifications of genes and gene expression. These studies may provide multiple sources of data pointing to the same gene or pathway, thus providing greater confidence in findings.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.