ReviewFrontiers in cardiovascular medicine2018
GWAS Reveal Targets in Vessel Wall Pathways to Treat Coronary Artery Disease.
Review in Frontiers in cardiovascular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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
12 citing papers in PubMed, 23 citations in OpenAlex.
- Gene regulatory network analysis identifies auranofin as an anti-atherosclerotic drug.Nature communications · 2026Article
- Genome-Wide Association Studies of Myocardial Infarction: A Systematic Literature Review.Journal of cardiovascular development and disease · 2026Review
- Gene editing therapy for cardiovascular diseases.MedComm · 2024Review
- Pharmacogenomics-based systematic review of coronary artery disease based on personalized medicine procedure.Heliyon · 2024Article
- Spontaneous Intracranial Hemorrhages in a Community of Asian Americans: Case Series and Literature Review.Cureus · 2024Article
- Review
- Coronary artery disease and cancer: a significant resemblance.Medical oncology (Northwood, London, England) · 2022Review
- Vascular smooth muscle cells in atherosclerosis: time for a re-assessment.Cardiovascular research · 2021Review
- Precision Medicine Approaches to Vascular Disease: JACC Focus Seminar 2/5.Journal of the American College of Cardiology · 2021Review
- Microanatomy of the Human Atherosclerotic Plaque by Single-Cell Transcriptomics.Circulation research · 2020Article
- Contributions of Interactions Between Lifestyle and Genetics on Coronary Artery Disease Risk.Current cardiology reports · 2019Review
- Genetic Insights Into Smooth Muscle Cell Contributions to Coronary Artery Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Coronary artery disease (CAD) is the leading cause of mortality worldwide and poses a considerable public health burden. Recent genome-wide association studies (GWAS) have revealed >100 genetic loci associated with CAD susceptibility in humans. While a number of these loci harbor gene targets of currently approved therapies, such as statins and PCSK9 inhibitors, the majority of the annotated genes at these loci encode for proteins involved in vessel wall function with no known drugs available. Importantly many of the associated genes linked to vascular (smooth muscle, endothelial, and macrophage) cell processes are now organized into distinct functional pathways, e.g., vasodilation, growth factor responses, extracellular matrix and plaque remodeling, and inflammation. In this mini-review, we highlight the most recently identified loci that have predicted roles in the vessel wall and provide genetic context for pre-existing therapies as well as new drug targets informed from GWAS. With the development of new modalities to target these pathways, (e.g., antisense oligonucleotides, CRISPR/Cas9, and RNA interference) as well as the computational frameworks to prioritize or reposition therapeutics, there is great opportunity to close the gap from initial genetic discovery to clinical translation for many patients affected by this common disease.
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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.