ReviewJournal of Taibah University Medical Sciences2017
The 9p21.3 risk locus for coronary artery disease: A 10-year search for its mechanism.
Review in Journal of Taibah University Medical Sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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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.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Decoding the shared genetic architecture of atherosclerotic cardiovascular disease: a genomic structural equation modeling analysis.BMC cardiovascular disorders · 2026Article
- What Causes Premature Coronary Artery Disease?Current atherosclerosis reports · 2024Review
- Epigenetics of hypertension as a risk factor for the development of coronary artery disease in type 2 diabetes mellitus.Frontiers in endocrinology · 2024Review
- Introducing Circulating Vasculature-Related Transcripts as Biomarkers in Coronary Artery Disease.Molecular diagnosis & therapy · 2023Article
- Lack of association between theJournal of Taibah University Medical Sciences · 2023Article
- Article
- Probing the epigenetic signatures in subjects with coronary artery disease.Molecular biology reports · 2020Article
- Association between Coronary Artery Disease and rs10757278 and rs1333049 Polymorphisms in 9p21 Locus in Iran.Reports of biochemistry & molecular biology · 2020Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 9p21.3 risk locus is the first locus to be associated with an increased risk of coronary artery disease (CAD)-related events and many other phenotypes. This locus contains 59 single nucleotide polymorphisms (SNPs) in a region with multiple long range enhancers and long non-coding RNAs (lncRNAs) that affect the expression of neighbouring genes, cyclin-dependent kinase 2A and 2B (CDKN2A and CDKN2B), which are required for controlling vascular smooth muscle cell proliferation and ageing. Several studies have attempted to identify the precise mechanism by which this locus exerts its pathogenic effect to increase the risk of CAD-related events. In this review, we will highlight the major advances in our understanding of the genotype-phenotype correlation at the mechanistic and phenotypic levels. The high population attributable risk of the 9p21.3 risk locus, mechanistic knowledge acquired thus far, and ongoing research efforts could facilitate the design of novel therapeutic molecules to reduce the risk of CAD and its related events.
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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.