ReviewCurrent atherosclerosis reports2013
Nutrigenetics and nutrigenomics of atherosclerosis.
Review in Current atherosclerosis reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Pooled it
- Association of the variants in the BUD13-ZNF259 genes and the risk of hyperlipidaemia.Journal of cellular and molecular medicine · 2014Trial
- Integrating (Nutri-)Metabolomics into the One Health Tendency-The Key for Personalized Medicine Advancement.Metabolites · 2023Review
- Genetics of Cardiovascular Disease: How Far Are We from Personalized CVD Risk Prediction and Management?International journal of molecular sciences · 2021Review
- Integrating systematic biological and proteomics strategies to explore the pharmacological mechanism of danshen yin modified on atherosclerosis.Journal of cellular and molecular medicine · 2020Article
- Nutrigenetics/Nutrigenomics, Personalized Nutrition, and Precision Healthcare.Current nutrition reports · 2020Review
- Role of Personalized Nutrition in Chronic-Degenerative Diseases.Nutrients · 2019Review
- Nutrigenetic Contributions to Dyslipidemia: A Focus on Physiologically Relevant Pathways of Lipid and Lipoprotein Metabolism.Nutrients · 2018Review
- Lipidomics: Techniques, Applications, and Outcomes Related to Biomedical Sciences.Trends in biochemical sciences · 2016Review
- Association between the MLX interacting protein-like, BUD13 homolog and zinc finger protein 259 gene polymorphisms and serum lipid levels.Scientific reports · 2014Article
- Aliphatic chain length by isotropic mixing (ALCHIM): determining composition of complex lipid samples by ¹H NMR spectroscopy.Journal of biomolecular NMR · 2014Article
- Consensus statement understanding health and malnutrition through a systems approach: the ENOUGH program for early life.Genes & nutrition · 2014Article
- Omega-3 supplementation reduces aggressive behavior: A meta-analytic review of randomized controlled trials.Aggression and violent behaviorArticle
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 at 2 institutions in 2 countries.
Funding
Abstract
The latest genome-wide association studies (GWAS) have re-energized our effort to understand the genetic basis of atherosclerotic cardiovascular disease. Although the knowledge generated by GWAS has confirmed that mediators of inflammation and perturbed lipid metabolism are major players in cardiovascular disease (CVD) development, much of individual disease heritability remains unexplained by the variants identified through GWAS. Moreover, results from interventions that aim at the pharmaceutical modification of lipid parameters fall short of expectation. These elusive treatment goals based on heritability studies highlight a key supportive, and perhaps even primary, role of nutritional therapy to achieve better health outcomes. Nonetheless, effective and specific interventions for CVD prevention using principles of "personalized" nutrition require a better knowledge of gene-diet interactions, an area that remains poorly explored. Dietary fatty acids such as omega-3 polyunsaturated fatty acids (PUFAs) are an excellent example of a widely studied "environment" that interacts with the genetic makeup in relation to CVD. A thorough exploration of the nutrigenomics and nutrigenetics of omega-3 PUFAs is key to understanding the etiology, and developing effective preventive measures. In this review, we will summarize the current state of knowledge of genetic interactions with omega-3 PUFAs in modulating lipid metabolism and inflammation, and defining health outcomes. Nutrigenetics and nutrigenomics are still in their infancy with respect to CVD prediction and therapy. Integration of the progress in the omics, including metabolomics, lipidomics, transcriptomics, and proteomics, coupled with advances in nutrigenomic and nutrigenetic research will move us towards personalized medicine as the ultimate paradigm of responsible clinical practice.
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.